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Table 1.  
Demographic and Clinical Characteristics
Demographic and Clinical Characteristics
Table 2.  
Comparison of Mean (SD) Sleep Parameter Findings on Preoperative and Postoperative Polysomnography
Comparison of Mean (SD) Sleep Parameter Findings on Preoperative and Postoperative Polysomnography
Table 3.  
Mean Sleep Parameter Changes by Demographic Characteristics
Mean Sleep Parameter Changes by Demographic Characteristics
Table 4.  
Mean Sleep Parameter Changes by Comorbidities
Mean Sleep Parameter Changes by Comorbidities
1.
Roland  PS, Rosenfeld  RM, Brooks  LJ,  et al; American Academy of Otolaryngology—Head and Neck Surgery Foundation.  Clinical practice guideline: polysomnography for sleep-disordered breathing prior to tonsillectomy in children.  Otolaryngol Head Neck Surg. 2011;145(1)(suppl):S1-S15.PubMedArticle
2.
Marcus  CL, Brooks  LJ, Draper  KA,  et al; American Academy of Pediatrics.  Diagnosis and management of childhood obstructive sleep apnea syndrome.  Pediatrics. 2012;130(3):576-584.PubMedArticle
3.
Tunkel  DE, Hotchkiss  KS, Carson  KA, Sterni  LM.  Efficacy of powered intracapsular tonsillectomy and adenoidectomy.  Laryngoscope. 2008;118(7):1295-1302.PubMedArticle
4.
Sterni  LM, Tunkel  DE.  Obstructive sleep apnea in children: an update.  Pediatr Clin North Am. 2003;50(2):427-443.PubMedArticle
5.
Bhattacharjee  R, Kheirandish-Gozal  L, Spruyt  K,  et al.  Adenotonsillectomy outcomes in treatment of obstructive sleep apnea in children: a multicenter retrospective study.  Am J Respir Crit Care Med. 2010;182(5):676-683.PubMedArticle
6.
Ye  J, Liu  H, Zhang  GH,  et al.  Outcome of adenotonsillectomy for obstructive sleep apnea syndrome in children.  Ann Otol Rhinol Laryngol. 2010;119(8):506-513.PubMedArticle
7.
Mitchell  RB.  Adenotonsillectomy for obstructive sleep apnea in children: outcome evaluated by pre- and postoperative polysomnography.  Laryngoscope. 2007;117(10):1844-1854.PubMedArticle
8.
Marcus  CL, Katz  ES, Lutz  J, Black  CA, Galster  P, Carson  KA.  Upper airway dynamic responses in children with the obstructive sleep apnea syndrome.  Pediatr Res. 2005;57(1):99-107.PubMedArticle
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Cullen  KA, Hall  MJ, Golosinskiy  A.  Ambulatory surgery in the United States, 2006.  Natl Health Stat Report. 2009;(11):1-25.PubMed
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Koltai  PJ, Solares  CA, Mascha  EJ, Xu  M.  Intracapsular partial tonsillectomy for tonsillar hypertrophy in children.  Laryngoscope. 2002;112(8, pt 2)(suppl 100):17-19.PubMedArticle
11.
Koltai  PJ, Solares  CA, Koempel  JA,  et al.  Intracapsular tonsillar reduction (partial tonsillectomy): reviving a historical procedure for obstructive sleep disordered breathing in children.  Otolaryngol Head Neck Surg. 2003;129(5):532-538.PubMedArticle
12.
Reilly  BK, Levin  J, Sheldon  S, Harsanyi  K, Gerber  ME.  Efficacy of microdebrider intracapsular adenotonsillectomy as validated by polysomnography.  Laryngoscope. 2009;119(7):1391-1393.PubMedArticle
13.
Du  W, Ma  B, Guo  Y, Yang  K.  Microdebrider vs. electrocautery for tonsillectomy: a meta-analysis.  Int J Pediatr Otorhinolaryngol. 2010;74(12):1379-1383.PubMedArticle
14.
Lister  MT, Cunningham  MJ, Benjamin  B,  et al.  Microdebrider tonsillotomy vs electrosurgical tonsillectomy: a randomized, double-blind, paired control study of postoperative pain.  Arch Otolaryngol Head Neck Surg. 2006;132(6):599-604.PubMedArticle
15.
Derkay  CS, Darrow  DH, Welch  C, Sinacori  JT.  Post-tonsillectomy morbidity and quality of life in pediatric patients with obstructive tonsils and adenoid: microdebrider vs electrocautery.  Otolaryngol Head Neck Surg. 2006;134(1):114-120.PubMedArticle
16.
Solares  CA, Koempel  JA, Hirose  K,  et al.  Safety and efficacy of powered intracapsular tonsillectomy in children: a multi-center retrospective case series.  Int J Pediatr Otorhinolaryngol. 2005;69(1):21-26.PubMedArticle
17.
Mitchell  RB, Kelly  J.  Outcome of adenotonsillectomy for severe obstructive sleep apnea in children.  Int J Pediatr Otorhinolaryngol. 2004;68(11):1375-1379.PubMedArticle
18.
Mitchell  RB, Kelly  J.  Outcome of adenotonsillectomy for obstructive sleep apnea in children under 3 years.  Otolaryngol Head Neck Surg. 2005;132(5):681-684.PubMedArticle
19.
Tauman  R, Gulliver  TE, Krishna  J,  et al.  Persistence of obstructive sleep apnea syndrome in children after adenotonsillectomy.  J Pediatr. 2006;149(6):803-808.PubMedArticle
20.
Guilleminault  C, Li  K, Quo  S, Inouye  RN.  A prospective study on the surgical outcomes of children with sleep-disordered breathing.  Sleep. 2004;27(1):95-100.PubMed
21.
Friedman  M, Wilson  MN, Friedman  J, Joseph  NJ, Lin  HC, Chang  HW.  Intracapsular coblation tonsillectomy and adenoidectomy for the treatment of pediatric obstructive sleep apnea/hypopnea syndrome.  Otolaryngol Head Neck Surg. 2009;140(3):358-362.PubMedArticle
22.
Guilleminault  C, Huang  YS, Glamann  C, Li  K, Chan  A.  Adenotonsillectomy and obstructive sleep apnea in children: a prospective survey.  Otolaryngol Head Neck Surg. 2007;136(2):169-175.PubMedArticle
23.
Friedman  M, Wilson  M, Lin  HC, Chang  HW.  Updated systematic review of tonsillectomy and adenoidectomy for treatment of pediatric obstructive sleep apnea/hypopnea syndrome.  Otolaryngol Head Neck Surg. 2009;140(6):800-808.PubMedArticle
24.
Costa  DJ, Mitchell  R.  Adenotonsillectomy for obstructive sleep apnea in obese children: a meta-analysis.  Otolaryngol Head Neck Surg. 2009;140(4):455-460.PubMedArticle
25.
Sorin  A, Bent  JP, April  MM, Ward  RF.  Complications of microdebrider-assisted powered intracapsular tonsillectomy and adenoidectomy.  Laryngoscope. 2004;114(2):297-300.PubMedArticle
26.
Mangiardi  J, Graw-Panzer  KD, Weedon  J, Regis  T, Lee  H, Goldstein  NA.  Polysomnography outcomes for partial intracapsular versus total tonsillectomy.  Int J Pediatr Otorhinolaryngol. 2010;74(12):1361-1366.PubMedArticle
27.
Thottam  PJ, Trivedi  S, Siegel  B, Williams  K, Mehta  D.  Comparative outcomes of severe obstructive sleep apnea in pediatric patients with trisomy 21.  Int J Pediatr Otorhinolaryngol. 2015;79(7):1013-1016.PubMedArticle
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Original Investigation
February 2016

Effectiveness of Powered Intracapsular Tonsillectomy in Children With Severe Obstructive Sleep Apnea

Author Affiliations
  • 1Department of Otolaryngology–Head and Neck Surgery, Thomas Jefferson University, Philadelphia, Pennsylvania
  • 2Office of Health Equity and Inclusion, Nemours/Alfred I. duPont Hospital for Children, Wilmington, Delaware
  • 3University of Maryland, College Park
  • 4Division of Pulmonary Pulmonology, Nemours/Alfred I. duPont Hospital for Children, Wilmington, Delaware
  • 5Division of Otolaryngology, Nemours/Alfred I. duPont Hospital for Children, Wilmington, Delaware
JAMA Otolaryngol Head Neck Surg. 2016;142(2):150-156. doi:10.1001/jamaoto.2015.3126
Abstract

Importance  Powered intracapsular tonsillectomy and adenoidectomy (PITA) is an increasingly common pediatric procedure. Few studies have examined its effectiveness in children with severe obstructive sleep apnea (OSA).

Objective  To assess the effectiveness of PITA in patients with severe OSA as evidenced by change in polysomnographic parameters.

Design, Setting, and Participants  We performed a case series study with medical record review of 70 children with severe OSA who underwent PITA at a tertiary care pediatric hospital from January 1, 2010, through December 31, 2014.

Main Outcomes and Measures  Preoperative and postoperative polysomnographic parameters.

Results  Of the 70 children with severe OSA who underwent PITA, 39 (56%) were boys, and the median age at surgery was 3.7 years. There were significant mean (SD) decreases in the postoperative apnea-hypopnea index (32.4 [28.4] vs 5.8 [9.7], P < .001), obstructive apnea index (20.4 [17.97] vs 2.55 [5.9]), obstructive apnea-hypopnea index (25.5 [22.4] vs 3.9 [7.3], P < .001), arousal index (53.7 [33.9] vs 27.4 [22.6], P < .001), percentage of total sleep time spent snoring (28.6 [30.5] vs 13.6 [20.8], P = .001), and oxygen desaturation index of 4% or more (22.9 [26.4] vs 4.5 [9.9], P < .001). Mean (SD) oxygen saturation (96.8 [2.0] vs 98.2 [1.3], P < .001) and oxygen saturation nadir (75.5 [13.1] vs 88.4 [8.1], P < .001) increased significantly. A significant decrease in time was observed with an end-tidal carbon dioxide greater than 55 mm Hg (49.67 [97.5] vs 19.1 [73.9] minutes, P = .01).

Conclusions and Relevance  Powered intracapsular tonsillectomy and adenoidectomy improved OSA in this series of pediatric patients by reducing obstructive apneas and hypopneas, oxygen desaturation, arousal index, carbon dioxide level, and snoring, as well as increasing oxygen saturation nadir. Results are comparable to those described for traditional electrocautery tonsillectomy and support the use of PITA for the treatment of severe OSA in children with adenotonsillar hypertrophy.

Introduction

Sleep-disordered breathing is common in the pediatric population, affecting approximately 12% of children. It is defined by an abnormal respiratory pattern during sleep and includes a spectrum of disorders ranging from mouth breathing and snoring to obstructive sleep apnea (OSA).1 Obstructive sleep apnea affects 1.2% to 5.7% of children,2 and as many as 40% of children referred to a sleep clinic or otolaryngologist for evaluation of sleep-disordered breathing will be diagnosed as having OSA.3,4 Adenotonsillar hypertrophy is the most common risk factor associated with pediatric OSA. Other risk factors include obesity, craniofacial syndromes, and neuromuscular disorders.2 Untreated OSA is associated with various comorbidities, including neurocognitive disturbances, behavior problems, cardiovascular disorders, failure to thrive, and systemic inflammation.2,57

Polysomnography is considered the criterion standard for diagnosing and quantifying OSA in children.1 Severity of OSA is graded based on the apnea-hypopnea index (AHI) and the oxygen saturation nadir. Mild OSA is defined as an AHI greater than 1 but 5 or less, moderate OSA as an AHI greater than 5 but 10 or less, and severe OSA as an AHI greater than 10 or an oxygen saturation nadir less than 80%.7 Dysfunction in neuromotor control is thought to be the underlying cause of airway collapse during sleep but is further exacerbated by airway narrowing associated with adenotonsillar hypertrophy.7,8 Enlarged upper airway tissues cause anatomical impingement of the upper airway and increase pharyngeal resistance, resulting in further episodic airway narrowing and collapse.

The American Academy of Pediatrics recommends adenotonsillectomy as the first line of treatment for OSA in children with adenotonsillar hypertrophy.2 In the United States, 530 000 cases of tonsillectomy with or without adenoidectomy are performed annually, making it the second most common ambulatory procedure performed in children 15 years and younger.9

Tonsillectomy is performed using various techniques. Traditional tonsillectomy is accomplished via sharp dissection or monopolar electrocautery to completely excise the tonsil with its surrounding capsule. In 2002, Koltai et al10 first described intracapsular tonsillectomy using a powered microdebrider, whereby the bulk of the tonsil tissue is removed while a small rim of tonsil tissue and the tonsillar capsule is preserved. Powered intracapsular tonsillectomy and adenoidectomy (PITA) is an effective technique for treatment of OSA in children. Studies revealed a reduction in postoperative AHI3 along with less postoperative pain and faster resumption of normal diet and activity compared with the traditional tonsillectomy using an electrocautery technique.1115 Children undergoing PITA have lower rates of postoperative bleeding and readmission for dehydration compared with those undergoing traditional tonsillectomy.16

Adenotonsillectomy improves OSA in most children; however, abnormal postoperative polysomnographic studies1720 have been reported in approximately 20% to 40% of cases. A severely elevated preoperative AHI is the most frequently reported risk factor for persistent elevation of AHI after tonsillectomy. Age, body mass index (calculated as weight in kilograms divided by height in meters squared), and presence of asthma (in nonobese children) are other reported risk factors.5,18,19 A paucity of literature exists on the outcomes of PITA in patients with severe OSA. The current study aimed to assess the effectiveness of PITA in patients with severe OSA using preoperative and postoperative polysomnographic parameters.

Methods

This retrospective cohort study (cases only) received Nemours Institutional Review Board approval before it was conducted. A sample of children who underwent intracapsular adenotonsillectomy for severe OSA from January 1, 2010, through December 31, 2014, was reviewed. A database of children who underwent polysomnography was searched for those who had severe OSA diagnosed by preoperative polysomnography, underwent PITA, and underwent postoperative polysomnography. Severe OSA was defined as an AHI greater than 10 or a nadir oxygen saturation level less than 80%. Intracapsular tonsillectomy involved removing approximately 90% of the tonsillar tissue via microdebrider, leaving the capsule intact. Suction electrocautery was then used to ablate the remaining tissue and to obtain hemostasis. Adenoidectomy was performed using suction electrocautery.

Demographic data collected included age at the time of surgery, sex, comorbidities, and body mass index. The following polysomnographic parameters were collected preoperatively and postoperatively: AHI, obstructive apnea index (OAI), obstructive AHI (OAHI), arousal index, mean and nadir oxygen saturation levels, oxygen desaturation index of 4% or higher, mean and maximum end-tidal carbon dioxide (etco2) levels, percentage of total sleep time (TST) with an etco2 level of 50 mm Hg or higher, time with an etco2 level of55 mm Hg or longer, and percentage of TST spent snoring.

Preoperative and postoperative polysomnographic parameters were compared using a paired t test. A univariable analysis was then performed using the correlated t test and Wilcoxon rank sum test to evaluate for any association between patient demographics and comorbidities and the observed change in each polysomnographic parameter. Patients were assessed for surgical cure based on several polysomnographic parameters. Mean preoperative OAI was compared among the patient groups with a postoperative OAI of 1 or less vs more than 1 using the 2-sample t test with unequal variance (2 sided). Mean preoperative AHI was compared among the patient groups with a postoperative AHI of 1 or less, an AHI of 2 or less, an AHI of 5 or less, and an AHI greater than 5 using the 1-way analysis of variance test. The significance level for all hypothesis tests was set at .05.

Results

Of the 70 children, 31 (44%) were girls and 39 (56%) were boys. The racial composition of the sample was 45.7% white, 41.4% African American, and 12.9% other. Median age at surgery was 3.7 years, whereas the median follow-up period was 0.7 years. Median interval between surgery and postoperative polysomnography was 5 months (range, 2-84 months). Patient comorbidities included reactive airway disease, asthma, gastroesophageal reflux disease, cardiac disease, neuromuscular disease, developmental delay, Down syndrome, craniofacial abnormalities, hematologic disorders, and obesity (Table 1).

There was a significant decrease in mean AHI, OAI, OAHI, arousal index, percentage of TST spent snoring, and oxygen desaturation index of 4% or higher on postoperative polysomnography. There was a significant increase in mean oxygen saturation and oxygen saturation nadir. We also noted a significant decrease in time with an etco2 level greater than 55 mm Hg (Table 2).

Reactive airway disease or asthma, gastroesophageal reflux disease, cardiac disease, developmental delay, Down syndrome, and craniofacial abnormalities did not appear to independently affect the degree of change in postoperative polysomnographic sleep parameters compared with patients without these comorbidities. Race, preoperative obesity, hematologic disease, and neuromuscular disease were found to affect the degree of change in postoperative polysomnography. In particular, African American patients had less improvement in arousal index compared with whites and those of other races. African Americans and people of other races had greater improvements in mean oxygen saturation (P = .02) and oxygen saturation nadir (P < .001) compared with whites (Table 3). Patients with neuromuscular disease experienced less improvement in in maximum etco2level (P = .05) and time with an etco2 level of 55 mm Hg or longer (P = .007) on postoperative polysomnography compared with patients without neuromuscular disease. Patients with hematologic disease similarly had significantly less improvement in mean oxygen saturation and oxygen desaturation index of 4% or higher on postoperative polysomnography compared with patients without hematologic disease. Preoperative obesity was associated with a greater improvement in postoperative mean oxygen saturation (P = .04) (Table 4). Sleep parameters not affected postoperatively by patient demographics or comorbidities included AHI, OAI, OAHI, mean etco2 level, percentage of TST with an etco2 level of 50 mm Hg or greater, and percentage of TST spent snoring.

Fifty patients (71%) achieved an OAI of 1 or less on postoperative polysomnography. Twenty-one patients (30%) achieved a postoperative AHI of 1 or less, 36 patients (51%) achieved a postoperative AHI of 2 or less, and 30 (43%) achieved an AHI greater than 1 but 5 or less, with an overall 51 (73%) achieving a postoperative AHI of 5 or less. In addition, 20 patients (29%) had a postoperative OAI greater than 1, and 19 patients (27%) had a postoperative AHI greater than 5. The mean preoperative OAI was 20.0 and 21.6 for patients with postoperative OAIs of 1 or less vs greater than 1, respectively. The differences between the mean preoperative OAIs did not significantly differ among the groups (P = .72). Mean preoperative AHI for patients with postoperative AHIs of 1 or less, 2 or less, 5 or less, or 5 or greater were 31.1, 35.2, 31.3, and 35.1, respectively. Preoperative AHI did not significantly differ among the postoperative AHI groups (P = .83).

Discussion

The purpose of this study was to assess the use of PITA as an effective technique for treating severe OSA in healthy patients and those with comorbidities. This study represents the largest cohort of patients with severe OSA (n = 70) and is the only study, to our knowledge, that includes patients with comorbidities who underwent PITA for OSA. Overall, our findings indicated improvement in multiple sleep parameters on postoperative polysomnography. Significant decreases in postoperative AHI, OAI, OAHI, arousal index, percentage of TST spent snoring, oxygen desaturation index of 4% or more, and time with an etco2 level of 55 mm Hg or more were found, as well as significant increases in mean oxygen saturation and oxygen saturation nadir. Because of the variability in the definition of surgical cure in the literature, we assessed the percentage cured based on the following parameters: OAI of 1 or less, AHI of 1 or less, AHI of 2 or less, and AHI of 5 or less. The highest cure rate (73%) was encountered when cure was defined as an AHI of 5 or less. The lowest cure rate (30%) encountered with surgical cure was defined as an AHI of 1 or less. The cure rates after PITA in patients with severe OSA and various comorbidities in this study are comparable to the cure rates reported in the literature (31%-70%) for generally healthy patients with severe OSA undergoing adenotonsillectomy (various techniques).6,12,17,21

Preoperative OAI and AHI were not found to be predictors of surgical success after PITA, suggesting the degree of AHI greater than 10 may not significantly affect surgical treatment outcomes. Presence of reactive airway disease or asthma, gastroesophageal disease, cardiac disease, developmental delay, Down syndrome, and craniofacial abnormalities did not appear to independently affect the degree of change in postoperative polysomnographic sleep parameters compared with patients without these comorbidities. The differences observed between improvements in arousal index, mean oxygen saturation, oxygen saturation nadir, oxygen desaturation index of 4 or higher, maximum etco2level, and time with an etco2 level longer than 55 minutes on postoperative polysomnography with various patient comorbidities (race, hematologic disease, obesity, and neuromuscular disease) suggest that aspects of the sleep profile may be affected by patient demographics and comorbidities.

Adenotonsillectomy is recommended as the first line of treatment for pediatric OSA in those children with adenotonsillar hypertrophy2; however, persistent OSA has been reported in approximately 20% to 40% of cases.1720 Challenges exist in assessing the rate of persistent OSA because of the lack of a consistent definition of cure as defined by polysomnography. Various reports57,12,19,21,22 have discussed a postoperative OAI of 1 or less, AHI of 1 or less, AHI of 2 or less, or AHI of 5 or less as a standard for cure. In a recent meta-analysis by Friedman et al,23 the cure rate of OSA after adenotonsillectomy was 66.3%, with cure rates defined per each study. When the cure rate was defined as an AHI less than 1, treatment success was 59.8%. If defined as an AHI less than 5, the cure rate was 66.2%. In patients with obesity, young age, and/or severe OSA, the mean cure rate was 38.7%. Overall, postoperative mean AHI was significantly decreased from preoperative levels. Types of adenotonsillectomy used were not described, and children with comorbidities aside from obesity were excluded from this meta-analysis. Elevated preoperative AHI and severity of OSA,57,21 patient age,5,18,19 body mass index and obesity,5,6,19,24 asthma,5 Friedman tongue position III or IV,21 Mallampati score of 3 to 4,22 nasal-septal deviation, and turbinate hypertrophy22 have been reported as significant predictors of persistent OSA after adenotonsillectomy.

PITA is a safe and effective technique for the treatment of pediatric OSA16 and is associated with decreased pain, bleeding risk, dehydration rate, and readmission rate compared with children undergoing conventional adenotonsillectomy.16,25 To date, 4 studies4,12,21,26 in the literature have evaluated the efficacy of PITA for treatment of pediatric OSA as evidenced by preoperative and postoperative polysomnography measures. Tunkel et al3 assessed 14 healthy children with moderate (n = 10) and severe OSA (n = 4) and noted a median decrease in AHI of 7.9 to 0.1 after PITA with a complete cure in 13 (93%) and partial cure in 1 (7%) (cure was defined as an AHI ≤1 and partial cure defined as an AHI ≤5). Friedman et al21 noted that a Friedman tongue position of III or IV and an elevated preoperative AHI of 20 or higher were independent predictors of poor treatment success after intracapsular coblation adenotonsillectomy in a retrospective review of 159 healthy children (43 of 159 had severe OSA, defined as an AHI ≥20) in 2009. Mean AHI decreased from 17.8 to 3.3, and 54.7% of patients achieved surgical cure, as defined by an AHI less than 1, with cure achieved in 22 patients (51%) with severe OSA. Within the same year, Reilly et al12 noted an overall decrease in mean AHI of 16.55 to 1.33 in 26 patients and a decrease of 23.7 to 1.45 in patients with severe OSA (n = 16). Complete cure was defined as an AHI of 1 or less and was achieved by 13 (50%) of the total cohort and 7 (44%) of those with severe OSA. Mangiardi et al26 found similar polysomnographic outcomes for children undergoing PITA vs traditional monopolar adenotonsillectomy; however, only approximately one-third of patients had an AHI less than 5 postoperatively. Of note, their cohort (n = 30) consisted of 70% overweight or obese children, whereas the previous 3 studies3,12,21 included 0% to 40% of overweight or obese children. Overall, studies3,12 assessing polysomnographic outcomes after intracapsular tonsillectomy have small sample sizes and lack assessments of children with comorbidities.

The current study found a mean (SD) postoperative AHI of 5.8 (9.7), which was improved from a mean (SD) preoperative value of 32.4 (28.4). The traditional and intracapsular tonsillectomy literature similarly supports the association between high preoperative AHI and persistent postoperative OSA.12,19,22 For instance, Mitchell7 found that persistent OSA, defined as an AHI of 5 or greater, was present in 12% with moderate preoperative OSA (AHI ≥10 but <20) and 36% of children with severe preoperative OSA (AHI ≥20). Ye et al6 similarly defined persistent OSA and noted that 4.4% of children with preoperative moderate OSA (AHI ≥10 but <20) and 30.0% of children with preoperative severe OSA (AHI ≥20) had an AHI of 5 or higher after adenotonsillectomy. Reilly et al12 defined resolution of OSA after intracapsular tonsillectomy as an AHI less than 1 and found that 56% of patients with preoperative severe OSA (AHI ≥10) had persistent mild OSA postoperatively. In a review by Thottam et al,27 nonsyndromic children with severe OSA (AHI ≥10) undergoing adenotonsillectomy had a mean postoperative AHI of 3.6, improved from 24.5. Resolution of OSA defined by complete resolution of symptoms was achieved in 75% of these children, leaving 25% of children with persistent symptoms. This literature has reported a range of mean postoperative AHIs of 1.45 to 6.5 in children with preoperative severe OSA.6,7,12,27 The cause of persistent OSA is likely multifactorial with variability from patient to patient. However, most commonly, additional and/or multilevel sites of obstruction remain present in the upper airway, contributing to persistent OSA.

Despite the strengths of this study—mainly large sample size and the assessment of various chronic comorbidities on treatment outcomes—there are some limitations. First, the assessment of PITA alone limited our ability to directly compare our results in this population with other tonsillectomy techniques. Second, follow-up polysomnography was typically performed at 2 months after surgery; however, this was not standardized because of the retrospective nature of the study. According to Friedman et al,21 patients with a longer duration from time of surgery to postoperative polysomnography had higher success rates. Therefore, variation in the postoperative polysomnographic results based on duration from time of surgery is possible. Third, our sample size, although the largest in the literature for this patient population, remains small.

A significant portion of children with severe OSA have persistent disease postoperatively, even when using the least strict criteria (postoperative AHI >5). Further research is needed to study even larger sample sizes of patients with severe OSA and comorbidities to elucidate their influence on persistent OSA.

Conclusions

PITA is an effective first-line surgical treatment for children with severe OSA and adenotonsillar hypertrophy. PITA improved OSA in our series of pediatric patients by reducing obstructive apneas and hypopneas, oxygen desaturation, arousal index, carbon dioxide level, and snoring and increasing oxygen saturation nadir. Results are comparable to those described for traditional electrocautery tonsillectomy and support the use of PITA for the treatment of severe OSA in children with adenotonsillar hypertrophy.

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Article Information

Submitted for Publication: August 3, 2015; final revision received September 21, 2015; accepted October 14, 2015.

Corresponding Author: Heather C. Nardone, MD, Nemours/Alfred I. duPont Hospital for Children, PO Box 269, Wilmington, DE 19899 (heather.nardone@nemours.org).

Published Online: December 30, 2015. doi:10.1001/jamaoto.2015.3126.

Author Contributions: Dr Nardone had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.

Study concept and design: LaHurd, Heinle, Nardone.

Acquisition, analysis, or interpretation of data: All authors.

Drafting of the manuscript: Mostovych, Holmes.

Critical revision of the manuscript for important intellectual content: Holmes, Ruszkay, LaHurd, Heinle, Nardone.

Statistical analysis: Holmes, LaHurd.

Administrative, technical, or material support: Mostovych, Heinle.

Study supervision: Holmes, Heinle, Nardone.

Conflict of Interest Disclosures: None reported.

Previous Presentation: This study was presented as a poster at the 2015 American Society of Pediatric Otolaryngology Annual Meeting; April 22-26, 2015; Boston, MA.

Additional Contributions: Li Xie, ScM, assisted with statistical analysis. No financial compensation was provided.

References
1.
Roland  PS, Rosenfeld  RM, Brooks  LJ,  et al; American Academy of Otolaryngology—Head and Neck Surgery Foundation.  Clinical practice guideline: polysomnography for sleep-disordered breathing prior to tonsillectomy in children.  Otolaryngol Head Neck Surg. 2011;145(1)(suppl):S1-S15.PubMedArticle
2.
Marcus  CL, Brooks  LJ, Draper  KA,  et al; American Academy of Pediatrics.  Diagnosis and management of childhood obstructive sleep apnea syndrome.  Pediatrics. 2012;130(3):576-584.PubMedArticle
3.
Tunkel  DE, Hotchkiss  KS, Carson  KA, Sterni  LM.  Efficacy of powered intracapsular tonsillectomy and adenoidectomy.  Laryngoscope. 2008;118(7):1295-1302.PubMedArticle
4.
Sterni  LM, Tunkel  DE.  Obstructive sleep apnea in children: an update.  Pediatr Clin North Am. 2003;50(2):427-443.PubMedArticle
5.
Bhattacharjee  R, Kheirandish-Gozal  L, Spruyt  K,  et al.  Adenotonsillectomy outcomes in treatment of obstructive sleep apnea in children: a multicenter retrospective study.  Am J Respir Crit Care Med. 2010;182(5):676-683.PubMedArticle
6.
Ye  J, Liu  H, Zhang  GH,  et al.  Outcome of adenotonsillectomy for obstructive sleep apnea syndrome in children.  Ann Otol Rhinol Laryngol. 2010;119(8):506-513.PubMedArticle
7.
Mitchell  RB.  Adenotonsillectomy for obstructive sleep apnea in children: outcome evaluated by pre- and postoperative polysomnography.  Laryngoscope. 2007;117(10):1844-1854.PubMedArticle
8.
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