What makes UpToDate so powerful?

  • over 11000 topics
  • 22 specialties
  • 5,700 physician authors
  • evidence-based recommendations
See more sample topics
Find Print
0 Find synonyms

Find synonyms Find exact match

Adenotonsillectomy for obstructive sleep apnea in children
Official reprint from UpToDate®
www.uptodate.com ©2017 UpToDate®
The content on the UpToDate website is not intended nor recommended as a substitute for medical advice, diagnosis, or treatment. Always seek the advice of your own physician or other qualified health care professional regarding any medical questions or conditions. The use of this website is governed by the UpToDate Terms of Use ©2017 UpToDate, Inc.
Adenotonsillectomy for obstructive sleep apnea in children
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2017. | This topic last updated: Jun 15, 2017.

INTRODUCTION — Obstructive sleep apnea (OSA) is common in the pediatric population. If untreated, the disease has been associated with a wide range of cardiovascular and cognitive morbidities [1-3]. Surgical removal of the tonsils and adenoids is considered the first-line treatment for OSA in otherwise healthy children over two years of age with adenotonsillar hypertrophy, as recommended in guidelines from the American Academy of Pediatrics (AAP) and the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) [4,5].

Adenotonsillectomy is one of the most common surgical procedures performed on children in the United States, with over 500,000 procedures performed annually [6]. The procedure is performed with increasing frequency for the indication of obstructive sleep-disordered breathing (SDB). In a survey of practice patterns by otolaryngologists in the United States, non-mutually exclusive indications for surgery included obstructed breathing of any type in 59 percent of cases, recurrent infections in 42 percent, and OSA in 39 percent of children; indicating that obstructed breathing now rivals recurrent infection as the most common surgical indication for adenotonsillectomy [7].

Although the majority of children undergoing adenotonsillectomy for SDB benefit from the procedure [8], the risk of complications or persistent disease after surgery mandates careful consideration of the risk-benefit ratio of surgical intervention for each individual patient. Moreover, children undergoing adenotonsillectomy for SDB should be evaluated postoperatively for symptom resolution to determine the need for additional evaluation or treatment [4].



Obstructive sleep-disordered breathing (SDB) includes a range of nocturnal breathing abnormalities, ranging from habitual snoring to frank OSA. Obstructive SDB is generally suspected initially based on symptoms and signs.

OSA is defined as periodic episodes of nocturnal airflow restriction (hypopneas) or obstruction (apneas) in association with sleep disruption, arousals from sleep, oxygen desaturation, and possible hypercapnia [4]. A polysomnogram (PSG, also known as a sleep study) is required for a definitive diagnosis of OSA.

The broad term "SDB" also encompasses non-obstructive causes of sleep-related breathing disorders, such as sleep-related hypoventilation disorders and central sleep apnea syndromes. In his topic review we will use the term "obstructive SDB" to describe signs and symptoms of nocturnal airway obstruction, with or without confirmation of OSA on PSG. For example, the term "obstructive SDB" as used here could include a child who snores and has hyperactive behavior during the day, but his or her PSG would not show, or does not show OSA.

Prevalence — Obstructive SDB is exceedingly common in the pediatric population. Peak incidence is between two and eight years of age, likely due to the relative size of lymphoid tissue in comparison with airway diameter. Reports of the prevalence of primary snoring in children range from 4 to 12 percent [9-12]. A systematic review of epidemiologic studies found an overall prevalence of parent-reported snoring by any definition of 7.45 percent [13]. Prevalence estimates for PSG-documented OSA in the general pediatric population have consistently ranged from 1 to 5 percent, based on cross-sectional studies [13-15].

High-risk populations — Children with obesity (especially if severe) are far more likely than lean children to have OSA, with reports of prevalence ranging from 13 to 59 percent [11,13,15,16]. A variety of congenital syndromes, craniofacial abnormalities, or neuromuscular disorders are also associated with a significantly increased risk for OSA, with prevalence estimates of 30 to 100 percent in Down syndrome, 15 percent in cerebral palsy, 85 percent in Pierre-Robin sequence, and over 50 percent in children with achondroplasia [17-22]. Micrognathia or midfacial hypoplasia are important predictors of OSA in infants, but isolated cleft palate probably is not. In a small prospective cohort study, infants with isolated cleft palate (confirmed by cephalometric findings) had similar polysomnographic findings compared with controls [23]. Children and adolescents with sickle cell disease have reduced upper airway diameters and increased adenoid and tonsil size (known risk factors for OSA) compared with normal volunteers [24]. Somewhat increased prevalence of OSA also has been reported in African-American children and in children with a history of prematurity compared with the general population. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Risk factors' and "Mucopolysaccharidoses: Clinical features and diagnosis" and "Overview of the pulmonary complications of sickle cell disease", section on 'Sleep disordered breathing'.)

SCREENING AND REFERRALS — Obstructive sleep-disordered breathing (SDB) is an important cause of morbidity in children. Untreated OSA may lead to growth failure, cognitive and behavioral abnormalities, and cardiovascular effects including cor pulmonale, right and left ventricular dysfunction, and systemic hypertension [1,2,9,25-28]. Less severe forms of obstructive SDB including primary snoring (snoring in the absence of OSA) have also been associated with decreased cognitive skills, diminished quality of life, and behavioral disturbances in children [4,28-31].

Initial screening — Because obstructive SDB is common and is an important cause of morbidity, all children should be screened for SDB as part of routine health care. The American Academy of Pediatrics (AAP) recommends the following steps at each well child visit [4]:

Ask the caregiver if the child snores and, if so, whether this is habitual (most nights), or only intermittent, and whether the snoring is loud.

If habitual or unusually loud snoring is reported, determine whether any of the following signs or symptoms are present:

Adenotonsillar hypertrophy (picture 1)

Obesity (especially if severe)

Mouth breathing

Long ("adenoidal") facies (picture 2)

Micrognathia, macroglossia, or other craniofacial abnormalities  


Morning headaches

Witnessed apneic episodes or gasping while sleeping, or "restless" sleep

Poor school function or daytime behavioral concerns (hyperactivity, sleepiness, or irritability)

Referral to an otolaryngologist or sleep specialist — If the child has snoring and one or more of these signs or symptoms, consideration should be given to a referral to an otolaryngologist (ear, nose, and throat specialist) or sleep specialist for further evaluation. Existing literature does not indicate which referral serves best. If polysomnography is indicated (PSG), this can be arranged by the specialist. Alternatively, the referring provider may be able to arrange for a PSG if a facility with experience in pediatric PSG is available; children with abnormal results of PSG or other significant sleep problems can then be referred to the appropriate specialist. (See 'Polysomnography' below.)

Referral to a tertiary care facility — Referral to a tertiary care center, or to a pediatric rather than a general otolaryngologist, should be considered (where available) for children with additional risk factors for complications of adenotonsillectomy. These include:

Severe sleep apnea (eg, PSG showing apnea-hypopnea index [AHI] ≥24 events per hour, oxygen saturation nadir of <80 percent, or peak PCO2 of ≥60 mmHg).

Difficult to manage airways due to anatomical abnormalities (eg, syndromes or congenital anomalies).

Increased potential for postoperative complications due to factors including severe obesity, very young age (eg, <24 months), craniofacial syndromes, neuromuscular disorders, coagulopathies, or other significant medical comorbidities.

In these cases, pediatric specialists and anesthesiologists or admission to a pediatric intensive care unit (PICU) for monitoring might be indicated [5].


Evaluation for OSA

History and physical examination — The physical examination by the specialist includes evaluation of tonsil size and adenoidal tissue. Tonsillar size is most often described on a scale from 0 to 5 (figure 1) [32]:

0 – Tonsils are entirely within the tonsillar pillar or previously removed by surgery.

1+ – Tonsils occupy 0 to 25 percent of the posterior pharynx.

2+ – Tonsils occupy 26 to 50 percent of the posterior pharynx.

3+ – Tonsils occupy 51 to 75 percent of the posterior pharynx.

4+ – Tonsils occupy 76 to 100 percent of the posterior pharynx (picture 3).

Indirect mirror examination of the nasopharynx and adenoid pad is often difficult in children. Direct fiber-optic transnasal laryngoscopy can be used as needed to assess adenoid size and the posterior or inferior extent of the pharyngeal tonsils, and can also identify other anatomical abnormalities such as lingual tonsillar hyperplasia or laryngomalacia. This procedure can generally be performed on awake children in the arms of their caregiver without sedation.

The child should be examined for a submucous cleft, which may be accompanied by a bifid uvula, midline deficiency or absence of muscular tissue, or a palpable notch in the hard palate. Children in whom submucous cleft of the palate is detected or those in whom velopharyngeal insufficiency is suspected (even if the examination is normal) should undergo additional evaluation by a specialist or a team skilled in cleft palate evaluation and management. In these children, standard adenoidectomy is often contraindicated due to an increased risk of developing velopharyngeal insufficiency. In these children, a limited or superior adenoidectomy is often performed.  

Although the history and physical examination by the specialist are important components of surgical planning, they are not sufficient to confirm or exclude the diagnosis of OSA in children with suggestive symptoms. As an example, parental reports of snoring and tonsillar size have high sensitivity but low specificity, whereas daytime somnolence or observed apneas had high specificity but low sensitivity [33]. Furthermore, a systematic review concluded that there is only a weak association between tonsil size (as evaluated by the physical examination) and OSA severity (as measured by polysomnography [PSG]) in the pediatric population [34]. Accordingly, in a systematic review, only 55 percent of children with suspected OSA on clinical evaluation subsequently had the disease confirmed when PSG was performed [35].

Questionnaires designed to assess nocturnal and daytime symptoms in children with suspected sleep-disordered breathing (SDB) are not sufficiently accurate to replace PSG in the clinical evaluation [36-39]. However, some questionnaires predict PSG results to an extent that is useful for clinical research, and other questionnaires may be useful to assess OSA-related behavioral issues and quality of life, and thereby help to determine the need for additional evaluation and support. At least two studies suggest that a pediatric OSA symptom inventory may predict some key outcomes of adenotonsillectomy more effectively than PSG [37,40]. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Questionnaires'.)

Polysomnography — Attended in-laboratory nocturnal PSG (overnight PSG) is considered the gold standard for diagnosis of OSA, as it is the only method able to definitively identify the presence of obstructive events and quantify the severity of OSA, including gas-exchange abnormalities and sleep disruption.

Higher-risk children – We suggest PSG prior to adenotonsillectomy for children with conditions that increase the risk of perioperative respiratory complications. These conditions include obesity (especially if severe), Down syndrome, craniofacial abnormalities, neuromuscular disorders, sickle cell disease, or mucopolysaccharidoses (table 1) [4,41]. The purpose of the PSG in these children is to improve diagnostic accuracy in high-risk populations and define the severity of OSA to optimize perioperative planning.  

Standard-risk children – For all other children, the necessity of preoperative PSG is controversial. Guidelines from the American Academy of Pediatrics (AAP) recommend that all children undergo PSG if this service is readily available, but acknowledge that alternative testing or referral to a specialist can be substituted [4]. By contrast, guidelines from the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) recommend PSG only if there is discordance between tonsil size and the reported severity of SDB symptoms [41].

The controversy arises from several recognized limitations of PSG: PSG has never been validated as a reliable tool to predict the risk of adverse outcomes of SDB or response to treatment [42]. There is also often a disparity between PSG measures and the severity of clinical symptoms. Children with severe daytime and nighttime symptoms may have a normal PSG, and snoring and symptoms of SDB have been associated with cognitive and behavioral abnormalities even in the absence of documented OSA on PSG [29-31]. Conversely, snoring children who are otherwise asymptomatic occasionally have severe respiratory disturbances on PSG [30]. Children with symptoms and signs of OSA, but negative PSGs, may still benefit from adenotonsillectomy [30]. Finally, pediatric PSG is expensive, labor-intensive, requires specially trained personnel, and may not be readily available in all areas.

In view of these limitations, it is not surprising that the use of PSG to confirm OSA prior to surgical intervention in clinical practice is somewhat selective, especially by otolaryngologists. In a 2004 practice pattern survey of pediatric otolaryngologists, 75 percent of respondents reported that they requested PSG in less than 10 percent of otherwise healthy children presenting with symptoms of SDB prior to performing adenotonsillectomy [43]. An updated internet practice survey conducted in 2013 showed that only 4 percent of pediatric otolaryngologists always referred children with SDB for PSG before performing adenotonsillectomy, 65 percent sometimes referred them, and 31 percent rarely or never referred them [44].  

Other diagnostic testing for OSA — If attended in-laboratory nocturnal PSG is not available, clinicians may consider alternate diagnostic tests including home sleep apnea tests, which are increasingly used in adults but are not adequately validated in children. Other alternatives to in-laboratory PSG include "nap" PSG, overnight continuous pulse oximetry, or audio- and video monitoring. All of these tests have a low negative predictive value, indicating that a negative result is insufficient to exclude OSA [45]. (See "Evaluation of suspected obstructive sleep apnea in children", section on 'Alternatives to PSG' and "Overview of polysomnography in infants and children", section on 'Alternative studies'.)  


Indications for surgery — The decision to initiate treatment for obstructive sleep-disordered breathing (SDB) is made on a case-by-case basis. Important considerations include the child's age, polysomnographic (PSG) abnormalities, and any underlying medical issues or complications related to OSA. Treatment decisions for children with OSA are discussed in more detail in a separate topic review. (See "Management of obstructive sleep apnea in children", section on 'Choice of therapy'.)

Adenotonsillectomy is generally considered first-line therapy for otherwise healthy children who have moderate or severe OSA and adenotonsillar hypertrophy. Adenotonsillectomy may also be initial therapy for children with multifactorial OSA, including contributions from obesity, if appreciable adenotonsillar tissue is present. OSA in obese children usually improves following adenotonsillectomy, although the outcome may be less satisfactory than in lean children. Finally, adenotonsillectomy should be considered in a child with OSA who does not have clear adenotonsillar hypertrophy. This is because in these circumstances the lymphoid tissue can still occupy a significant proportion of the potential upper airway.

Children with Down syndrome, craniofacial anomalies, neuromuscular disorders, or mucopolysaccharidoses typically have multifactorial OSA, with airway obstruction at multiple sites. They are therefore more likely to have respiratory complications in the perioperative period, and to have persistent OSA after adenotonsillectomy, as discussed below. Nonetheless, adenotonsillectomy is often the most appropriate initial therapy for these children if appreciable adenotonsillar tissue is present, and usually leads to improvement in OSA, even if the OSA does not fully resolve [46]. Medical therapy and/or adjuvant surgical procedures are used as alternatives or supplements to adenotonsillectomy, depending on the severity and specific locations of airway obstruction in the individual patient, and on associated comorbidities. (See 'Risk factors for persistent disease' below and 'Management of patients with residual OSA after adenotonsillectomy' below.)

Relative contraindications to adenotonsillectomy include little or no adenotonsillar tissue, submucous cleft palate, a bleeding disorder that cannot be adequately controlled for surgery, or other underlying disorders that render the patient medically unstable for surgery [4].

Alternatives to adenotonsillectomy:

Watchful waiting for several months may be an acceptable alternative for otherwise healthy children with mild or moderate OSA without significant oxygen desaturation and with tolerable symptomatology. If this approach is chosen, the child should be reevaluated within six months for worsening of clinical symptoms, or reevaluated sooner if symptoms worsen. (See "Management of obstructive sleep apnea in children", section on 'Choice of therapy'.)

Positive airway pressure therapy can be used when adenotonsillectomy is contraindicated (eg, due to comorbid diseases that increase the risk of surgery). It can also be employed when a patient with OSA has minimal adenotonsillar tissue, persistent OSA despite adenotonsillectomy, or a strong preference for a nonsurgical approach. (See "CPAP for pediatric obstructive sleep apnea", section on 'Treatment decisions'.)

Weight loss is recommended as an adjunctive therapy for obese children with OSA because obesity contributes to the increased upper airway resistance. However, adenotonsillectomy also should be performed if there is even mild adenotonsillar hypertrophy.

Other interventions for selected children with OSA include rapid maxillary expansion (RME), corticosteroids/antiinflammatory therapy, and positional therapy. (See 'Rapid maxillary expansion' below and "Management of obstructive sleep apnea in children", section on 'Other adjunct therapies'.)

Preoperative assessment — The history should explore symptoms of unusual bleeding or bruising, or a family history of bleeding disorders.

Routine laboratory testing such as coagulation studies (prothrombin time [PT], activated partial thromboplastin time [aPTT], international normalized ratio [INR], platelet count) is not necessary unless the history suggests the possibility of a bleeding disorder. Although hemorrhage is an important complication after adenotonsillectomy, multiple studies have found that preoperative coagulation evaluation is not effective in identifying those children who will have postoperative hemorrhage. (See "Tonsillectomy and/or adenoidectomy in children: Preoperative evaluation and care", section on 'Hematologic evaluation'.)

Similarly, children do not require routine preoperative cardiac evaluation before adenotonsillectomy unless there are known cardiac abnormalities or comorbidities. Although severe OSA is associated with hypertension and cardiac dysfunction, preoperative testing such as echocardiography is not helpful in predicting which children will develop perioperative complications [47]. (See "Tonsillectomy and/or adenoidectomy in children: Preoperative evaluation and care", section on 'Cardiac evaluation'.)

If PSG was not already performed for diagnostic purposes, it is recommended for preoperative planning for patients with conditions that increase the risk for respiratory complications, including obesity, Down syndrome, craniofacial abnormalities, neuromuscular disorders, sickle cell disease, or mucopolysaccharidoses, as discussed above (see 'Polysomnography' above). When severe OSA is suspected clinically, PSG documentation of severity is sometimes used to justify overnight admission after surgery rather than same-day discharge. This is because of increased risk for postoperative respiratory complications in patients with severe OSA. (See 'Operative setting' below.)

Children with the following disorders require additional evaluation and disease-specific management (see "Tonsillectomy and/or adenoidectomy in children: Preoperative evaluation and care", section on 'Preoperative care in specific patient populations'):

Bleeding disorders (eg, Von Willebrand disease or platelet function defects)

Sickle cell disease – because of risks for complications including acute chest syndrome in the perioperative period

Down syndrome – to assess for possible atlantoaxial instability or hypothyroidism and manage anesthesia-related respiratory complications

Operative setting — For the majority of children, adenotonsillectomy can be safely performed in an ambulatory setting. Indications for overnight hospitalization after tonsillectomy include a complex medical history; a history of severe OSA (defined in this case as an apnea-hypopnea index [AHI] of >10, oxygen saturation nadir less than 80 percent, or both); or age younger than three years [5,41]. For children younger than three years whose OSA is not severe and who have no other risk factors, complication rates are low, and the need for inpatient admission has been questioned [48]. (See "Tonsillectomy (with or without adenoidectomy) in children: Postoperative care and complications", section on 'Inpatient admission'.)

Guidelines and clinical practice vary regarding indications for performing adenotonsillectomy in a tertiary care setting and for postoperative admission to a pediatric intensive care unit (PICU) or extended observation in a postanesthesia care unit (PACU). These precautions are usually recommended for children with very severe OSA, very young children (eg, <24 months), cardiac complications of OSA, failure to thrive, severe obesity, craniofacial or chromosomal anomalies, neuromuscular disorders, or current upper respiratory infections [45]. However, the threshold for defining very severe OSA varies. Suggested criteria include AHI ≥24; rapid eye movement (REM) AHI ≥60 [49]; and/or oxygen saturation nadir <70 percent [50].

Perioperative medications — Perioperative medications, including the use of dexamethasone to prevent postoperative nausea, and pain management are discussed in a separate topic review. (See "Anesthesia for tonsillectomy with or without adenoidectomy in children", section on 'Antiemetics' and "Anesthesia for tonsillectomy with or without adenoidectomy in children", section on 'Analgesia'.)

The use of antimicrobial prophylaxis at the time of, or for short periods following, adenotonsillectomy does not improve postoperative outcomes and is not recommended [5,51]. (See "Tonsillectomy (with or without adenoidectomy) in children: Postoperative care and complications", section on 'Antimicrobial prophylaxis'.)

Surgical techniques — A variety of instruments have been devised for the removal of tonsillar and adenoid tissue. Traditionally, the most common approach has been extracapsular (complete) tonsillectomy, but intracapsular (partial) tonsillectomy is increasingly used.

Extracapsular tonsillectomy — Extracapsular tonsillectomy (also known as complete, total, or sub-capsular tonsillectomy) consists of removal of the entire palatine tonsil and the surrounding fascia or capsule with either cold or hot techniques (figure 2 and picture 1).

For "cold" or sharp dissection, the mucosa is sharply excised from the tonsillar pillar with a scissor or scalpel and then blunt instruments are used to divide the tonsillar capsule from the underlying musculature. Hemostasis is then achieved with a combination of pressure, cautery, ligation, or hemostatic agents.

For "hot" techniques, electrosurgical or thermal instruments are utilized to excise the tonsillar tissue (movie 1). A variety of instruments and technologies have been developed for this purpose including monopolar electrocautery (Bovie), lasers, diathermy, bipolar electrosurgical scissors or forceps, and bipolar radiofrequency ionic dissociation. Hot techniques allow for simultaneous cauterization of blood vessels and enable surgeons to perform the procedure quickly and with minimal blood loss in most cases.

Each of these approaches has advantages. Hot techniques allow for simultaneous cauterization of blood vessels and enable surgeons to perform the procedure quickly and with minimal blood loss in most cases. On the other hand, some studies have shown that use of cold dissection and radiofrequency techniques are associated with less pain and more rapid return to normal function. As an example, a systematic review comparing cold dissection with diathermy tonsillectomy in 254 patients found that the diathermy group had reduced intraoperative bleeding, but increased pain [52]. Therefore, none of the more current clinical guidelines advocate for use of any one specific surgical technique for extracapsular tonsillectomy over others, and the decision of which technique to use is generally based on surgeon preference and training [53].

Intracapsular tonsillectomy (tonsillotomy) — Intracapsular tonsillectomy (also known as subtotal or partial tonsillectomy, or "tonsillotomy") is increasingly used for the treatment of obstructive SDB. In this technique, microdebriders, bipolar electrosurgical scissors, or radiofrequency ablation (including "coblation") devices are used to debulk the obstructing portions of the tonsil parenchyma [54-56]. Some evidence suggests that the technique permits more rapid recovery compared with traditional tonsillectomy, and possibly reduces the risk of postoperative hemorrhage. However, there is a risk of tonsillar regrowth, which usually is clinically insignificant but occasionally requires revisional surgery.

The evidence that this technique permits more rapid recovery comes from multiple randomized trials comparing adenotonsillectomy techniques for children with SDB. As an example, a randomized study with 156 patients compared treatment with intracapsular tonsillectomy with microdebrider, intracapsular tonsillectomy with coblation, and traditional extracapsular tonsillectomy with electrocautery dissection [57]. Patients undergoing intracapsular tonsillotomy with either coblation or microdebrider returned to a normal diet and activity between one and two days earlier than those undergoing extracapsular tonsillectomy, and the subgroup using coblation required pain medication for two days fewer than patients in the other groups. There were no statistically significant differences in postoperative complications between the three techniques. Similarly, in a systematic review that included 16 randomized studies, pooled data analysis demonstrated that length of time until pain was absent was superior with intracapsular tonsillectomy, compared with traditional extracapsular tonsillectomy [58].

The evidence regarding postoperative hemorrhage is somewhat weaker. The above systematic review concluded that intracapsular tonsillectomy was associated with marginally decreased rates of postoperative hemorrhage compared with extracapsular tonsillectomy [58], while a separate review found no difference in postoperative hemorrhage or dehydration among high-quality studies [59].

Reported rates of tonsillar regrowth after intracapsular tonsillectomy range from 0.5 to 16.6 percent, which is of particular concern when the technique is used for treatment of SDB [60-63]. The regrowth occasionally is clinically significant. As an example, one study reported regrowth in 7 of 42 children after intracapsular tonsillectomy (16.6 percent), and 5 of these children required revision tonsillectomy (12 percent overall) [62]. In a randomized trial of intracapsular tonsillectomy versus extracapsular tonsillectomy for OSA, initial outcomes were similar [63]. However, 5 of 39 (13 percent) children who underwent intracapsular tonsillectomy for OSA needed repeat surgery for regrowth and recurrence of OSA, compared with 0 of 40 children who underwent extracapsular tonsillectomy.

In view of these potential benefits and uncertainties, intracapsular tonsillectomy is often but by no means universally used for surgical treatment of obstructive SDB in children. In a practice pattern survey of pediatric otolaryngologists in the United States, 73 percent of surgeons reported always performing complete extracapsular tonsillectomy for a surgical indication of SDB [64].

Adenoidectomy — During adenoidectomy, the obstructing portions of adenoid tissue are removed from the nasopharynx with the use of ether sharp curettes (sharp or cold dissection), electrocautery, coblation, or microdebrider (picture 4). The procedure is generally done trans-orally after retraction of the soft palate, taking care to avoid trauma to the undersurface of the palate or Eustachian tube orifices. Occasionally, tissue removal via a trans-nasal approach also may be necessary.

Complications of adenotonsillectomy — The vast majority of children will have throat pain, otalgia, halitosis, and odynophagia after adenotonsillar surgery and for up to two weeks until the tonsillar fossae are fully mucosalized. Transient nausea and vomiting are not uncommon, sometimes requiring admission or readmission for dehydration [65]. Good hydration is associated with decreased postoperative pain, and immediate resumption of oral intake after surgery should be encouraged [66]. Post-tonsillectomy bleeding can occur either within 24 hours (termed early, immediate, or primary hemorrhage) or at any subsequent time (termed delayed or secondary hemorrhage). Primary hemorrhage typically ranges from 0.2 to 2.2 percent and secondary hemorrhage between 0.1 and 3 percent [67]. (See "Tonsillectomy (with or without adenoidectomy) in children: Postoperative care and complications", section on 'Complications'.)

Postoperative respiratory complications are also frequent after adenotonsillectomy and can range from transient laryngospasm or mild desaturation requiring patient repositioning or supplemental oxygen, to life-threatening airway obstruction or pulmonary edema. OSA is an important risk factor for developing postoperative respiratory complications, particularly if the OSA is severe [68]. Other risk factors include cardiac morbidity (due to the OSA or other factors), obesity, craniofacial or neuromuscular disorders, history of seizures, asthma or prematurity, or recent upper respiratory infections [69]. Children with any of these risk factors should be carefully observed for respiratory complications during the postoperative period. (See "Tonsillectomy (with or without adenoidectomy) in children: Postoperative care and complications", section on 'Respiratory complications'.)


Success rates — Most otherwise healthy children with obstructive sleep-disordered breathing (SDB) and adenotonsillar hypertrophy will benefit from adenotonsillectomy, as measured by polysomnography (PSG) and symptoms.

Polysomnographic outcomes — Reported PSG outcomes after adenotonsillectomy for children with OSA vary considerably, with reported success rates ranging from 27 to 80 percent, depending on study design and PSG criteria used to define a successful outcome [8,70-72]. The PSG outcomes are illustrated by the following studies:

A randomized trial compared the outcomes of adenotonsillectomy with those of watchful waiting and supportive care (Childhood Adenotonsillectomy Trial [CHAT] trial) [8]. The subjects were 464 children, five to nine years of age with PSG-documented OSA (apnea-hypopnea index [AHI] 2 to 30 events/hour) without significant oxygen desaturation. At seven month's follow-up, 79 percent of children treated with adenotonsillectomy had normalization of PSG findings, compared with 46 percent of the group who did not undergo surgery. Resolution of OSA was less common in children with obesity and higher AHI at baseline. Of note, children with severe OSA and significant comorbidities or syndromes were excluded from this study.

In a meta-analysis of studies involving over 1000 children who underwent tonsillectomy for OSA, 59 percent had complete normalization of PSG parameters, defined by AHI <1 [72]. The resolution rate was 39 percent in patients with severe obesity or severe OSA, compared with 74 percent in uncomplicated patients.

In a retrospective multisite study involving 578 children, only 27 percent had resolution of OSA using the same criteria, although significant reduction in mean AHI was seen (from 18.2 ± 21.4 to 4.1 ± 6.4 events per hour) [71]. The lower rate of resolution in this trial may be explained by the characteristics of the study population, which was enriched in characteristics associated with residual disease following adenotonsillectomy, including older age, obesity, or more severe OSA at baseline (AHI >5).

Symptomatic outcomes

Quality of life — There is moderately good evidence that adenotonsillectomy improves quality of life for children with OSA [73]. The best evidence for short-term improvement is from the randomized CHAT trial described above [8,74]. The group treated with adenotonsillectomy experienced greater improvements in several standardized measures of quality of life and sleep quality, although improvements in OSA severity explained only a small portion of the observed changes. Similarly, a meta-analysis of observational studies found improvements in a disease-specific quality of life survey, and these improvements persisted in longer-term follow-up [75].

Cognitive and behavioral — There is somewhat weaker evidence that adenotonsillectomy may improve cognitive function and behavior in children with OSA. Observational studies have reported postoperative improvements in objective measures of impulsivity, inattention, and cognitive function after adenotonsillectomy [30,76,77], or in behavior reported by their parents [78]. In the randomized CHAT trial described above, children treated with adenotonsillectomy had improvement in behaviors as reported by their parents and teachers, but no differences in an objective measure of attention and executive functioning, which was the primary outcome [8]. (See "Cognitive and behavioral consequences of sleep disorders in children", section on 'Sleep-related breathing disorders'.)

Risk factors for persistent disease — Although adenotonsillectomy improves PSG measures in most children with OSA, a substantial proportion of patients have persistent disease, ranging from 13 to 79 percent depending on the criteria used to define persistent disease and the study population [4]. Recurrence of OSA can also be seen long after adenotonsillectomy, even when initial resolution of disease was achieved. As an example, in a prospective study of 62 children ages 7 to 13 years who underwent adenotonsillectomy for documented OSA, postoperative PSGs were obtained at six weeks, six months, and one year after surgery [79]. A trend toward increasing AHI was seen in the period from six months to one year after surgery; obesity, African American race, and rapid increase in body mass index (BMI) were risk factors for recurrent OSA. In a separate prospective longitudinal study of 135 children undergoing adenotonsillectomy for documented OSA, a worsening of postoperative AHI was seen in 68 percent of children during the 36 month follow-up period [80].

The likelihood of persistent disease is increased in the patients with the following characteristics [71,81-87]:


More severe OSA at baseline

Craniofacial anomalies, Down syndrome, or mucopolysaccharidoses

The increased rates of persistent disease among children with obesity was demonstrated by a meta-analysis of adenotonsillectomy outcomes in children with obesity [84]. Although most children had improvement in their OSA postoperatively, only half had postoperative AHI <5, and one-quarter had postoperative AHI <2. Among children with Down syndrome, up to 73 percent have persistent OSA requiring additional therapy [85].  

Indications for postoperative polysomnography — We recommend a clinical reevaluation of all children several months after adenotonsillectomy to determine whether snoring and other symptoms of SDB have resolved. For those with persistent symptoms or concerns, we suggest proceeding to postoperative PSG. In children with higher risk of persistent disease, such as those with severe obesity or craniofacial syndromes, a postoperative PSG should be considered even in the absence of snoring or other symptoms [4].

In clinical practice, postoperative testing is generally performed several months after surgery to ensure stable healing of the operative site. No studies to date have evaluated the timing of postoperative PSG evaluation, and this issue is not specifically addressed in practice guidelines regarding management of pediatric OSA.

Weight gain — The relationship between OSA, adenotonsillectomy, and weight gain is complex. In some cases, OSA appears to restrict weight gain in some children, and adenotonsillectomy can reverse the restriction or promote weight gain, at least in the short term [88]. In a retrospective case-control series of 154 children undergoing adenotonsillectomy and 182 controls, those children undergoing surgery gained more weight over the subsequent two years. A statistically significant increase in weight was seen the obese children after surgery, but not in those who were overweight or of normal weight at baseline [89]. In the CHAT trial, weight gain was also greater in children who had early adenotonsillectomy compared with the observation-only controls [90]. Furthermore, children who were overweight (but not those who were normal weight or underweight) prior to surgery were more likely to become obese by the seven-month follow-up, compared with children who did not undergo surgery. Among children who were overweight at baseline who underwent adenotonsillectomy, 52 percent became obese at follow-up, compared with 21 percent in the watchful waiting group. Thus, when children at risk for overweight or obesity require treatment for OSA by adenotonsillectomy, care should be taken to minimize or reverse anticipated weight gain. (See "Definition; epidemiology; and etiology of obesity in children and adolescents", section on 'Sleep' and "Evaluation of suspected obstructive sleep apnea in children", section on 'Examination'.)


Diagnostic procedures — Patients with clinically significant OSA after adenotonsillectomy should be further evaluated to determine the site(s) of obstruction and guide further interventions. In most cases, the first step is flexible fiber-optic nasolaryngoscopy, which may identify nasopharyngeal stenosis, lingual tonsillar hypertrophy, or laryngomalacia. If more information is needed, drug-induced sleep endoscopy (DISE) or cine magnetic resonance imaging (MRI) can help to identify specific sites of obstruction.  

Drug-induced sleep endoscopy — DISE, also known as drug-induced sedation endoscopy, is a commonly used procedure for evaluating patients with residual OSA. This consists of assessment of the entire airway using a flexible fiber-optic laryngoscope during anesthetically-simulated sleep with preservation of spontaneous respiration. DISE is increasingly being utilized to evaluate site of airway collapse prior to surgical intervention in children anatomically predisposed to multilevel collapse, or in those with persistent OSA after adenotonsillectomy [91-94].

DISE evaluates the extent and orientation of obstruction at four to five anatomical sites of potential collapse (adenoids, palate or velum, lateral pharyngeal wall, tongue base, and epiglottis or supraglottis). The scoring systems have substantial intra- and interrater agreement (>0.6), and children with multilevel obstruction tend to have more severe OSA as measured by polysomnography (PSG) [95,96]. In a study of 82 children with mild-severe OSA, DISE revealed oropharyngeal and lateral wall collapse in most patients (72 of 82), and the majority had obstruction at multiple sites [97]. In a separate study, DISE-directed surgery led to significant improvements in the apnea-hypopnea index (AHI) among 41 children with persistent OSA following adenotonsillectomy (AHI decreasing from 15.7 to 7.9 events per hour), and also in 39 children who had not previously undergone adenotonsillectomy (AHI decreasing from 13.8 to 8.0 events per hour) [91]. Larger studies are needed to better evaluate the success and utility of DISE-directed surgery to address OSA in children.  

Magnetic resonance imaging — Cine MRI is done under sedation and allows for three-dimensional analysis of the upper airway. This technique is useful for surgical planning in children in whom multiple sites of obstruction are suspected due to obesity, craniofacial syndromes, or neuromuscular disorders, or in children with persistent OSA after adenotonsillectomy [98]. As an example, in a group of 27 patients with Down syndrome and persistent OSA after adenotonsillectomy, cine MRI identified multiple sites of anatomical collapse, including glossoptosis and recurrent adenoid tissue (each in 63 percent of patients), hypopharyngeal collapse (22 percent), lingual tonsillar hypertrophy (30 percent), and macroglossia (74 percent) [99].

Non-surgical therapeutic options

Watchful waiting — In children with mild residual OSA after adenotonsillectomy but few or no symptoms, continued observation may be appropriate, as suggested by data on watchful waiting for children who have not had surgery. Asymptomatic children with mild residual OSA after adenotonsillectomy may not require active intervention. (See "Management of obstructive sleep apnea in children", section on 'Choice of therapy'.)

Weight loss — Weight loss has been demonstrated to reduce severity of OSA in obese adults [100]. Less evidence is available regarding the impact of weight loss, exercise programs, or diet on OSA for obese children and adolescents. Nonetheless, given the strong association between obesity and OSA in children, children with obesity and residual OSA after adenotonsillectomy should be encouraged to lose weight and offered support to assist these efforts. Weight loss surgery also may be an option for adolescents with severe obesity and OSA and/or other obesity-associated morbidities.

Several studies in obese children and adolescents suggest that OSA is likely to improve if weight loss can be achieved. In a study of 31 obese teenagers in a residential weight loss program, 62 percent had resolution of obstructive symptoms after a median weight loss of 24.0 kg, prompting a conclusion that weight loss was a successful treatment option for OSA in obese teenagers [101]. This is supported by a study of 34 obese teenagers undergoing weight loss surgery, of whom 19 children had moderate OSA (AHI >5) preoperatively. Of the 10 children for whom postoperative PSG data was available, the mean AHI decreased from 9.2 to 0.62 events/hour [102]

Medical therapy — Intranasal corticosteroids or leukotriene modifier therapy have been used primarily to treat mild OSA as an alternative to adenotonsillectomy or continuous positive airway pressure (CPAP) therapy. Their use in children who have not undergone adenotonsillectomy is discussed separately [103-105]. (See "Management of obstructive sleep apnea in children", section on 'Corticosteroids/Antiinflammatory therapy'.)

These medical therapies may also be helpful in children with mild residual OSA after adenotonsillectomy, especially if concurrent nasal obstruction is present. In one study, children with mild residual OSA after adenotonsillectomy experienced modest improvement after treatment with the combination of montelukast and intranasal budesonide for 12 weeks, compared with controls who had residual OSA but were not treated with medical therapy [106].

Rapid maxillary expansion — Rapid maxillary expansion (RME) is an orthodontic treatment in which a dental appliance contacts the hard palate and is held in position by connections to the posterior teeth (picture 5). The appliance is gradually expanded, which widens the palate and nasal passages, thereby increasing airway patency and reducing nocturnal obstruction. The technique is used prior to midline fusion of the maxilla, which generally occurs shortly prior to puberty. RME can be used for children with OSA and narrow palate (crossbite) who have little adenotonsillar tissue, or for those with residual OSA after adenotonsillectomy. (See "Management of obstructive sleep apnea in children", section on 'Orthodontics'.)

Positive airway pressure — Continuous positive airway pressure (CPAP) and bilevel positive airway pressure (BPAP) therapy have been used successfully in many children with OSA. They are generally effective, but adherence to therapy can be challenging as in adults, and its use requires a motivated family. Given the problems with adherence and high frequency of improvement by adenotonsillectomy, positive airway pressure is typically reserved for children who have significant residual OSA after surgical intervention, or for those who are not considered appropriate surgical candidates. The use of CPAP or BPAP in children with OSA is discussed in more detail in a separate topic review. (See "CPAP for pediatric obstructive sleep apnea".)  

CPAP or BPAP are sometimes used to provide temporary airway support in selected patients in the immediate postoperative period after adenotonsillectomy, as documented in a small case series of nine children with medical comorbidities undergoing adenotonsillectomy [107].

Adjuvant surgical procedures — Surgical procedures other than adenotonsillectomy are sometimes considered to treat OSA in children without significant tonsillar hypertrophy, or with residual disease after adenotonsillectomy. These adjuvant surgical procedures may also be beneficial in patients with a high probability that OSA is due to factors other than adenotonsillar hypertrophy alone, such as in children with obesity, Down syndrome, craniofacial syndromes, or neuromuscular disease.

In these cases, additional evaluation to determine site of obstruction is often helpful. Flexible fiberoptic nasolaryngoscopy may identify nasopharyngeal stenosis, lingual tonsillar hypertrophy, or laryngomalacia. DISE and cine MRI are increasingly used to identify the site of airway obstruction during sleep and assist in surgical planning for children with residual OSA after adenotonsillectomy. (See 'Drug-induced sleep endoscopy' above and 'Magnetic resonance imaging' above.)

Tongue base procedures — Airway obstruction at the level of the base of tongue is increasingly recognized as a cause of persistent OSA after adenotonsillectomy, especially in children with obesity, Down syndrome, and craniofacial or neuromuscular disorders [91,92,95,97-99]. The site of obstruction is often identified by fiberoptic nasolaryngoscopy, cine MRI or DISE, as discussed above. (See 'Diagnostic procedures' above.)

Previous methods to reduce tongue tissue, primarily with the use of lasers, were limited by morbidity and not widely performed [108]. Newer minimally invasive techniques and technical advancements have made these techniques more accessible and have increased patient acceptance. Several small studies have evaluated the use of procedures to reduce tongue tissue, advance tongue musculature, or ablate lingual tonsil tissue to address collapse at this site in children, as illustrated by the following case series:

Endoscopic-assisted coblation lingual tonsillectomy has emerged as a safe and effective technique to treat tongue base collapse in children with OSA. A retrospective case series described the use of this technique in 26 patients with PSG-documented OSA after adenotonsillectomy in whom obstructive lingual tonsillar hypertrophy was identified by DISE [109]. The procedure resulted in significant reduction in the mean obstructive apnea index (OAI) from 18.1 to 2.2 events/hour. Two patients developed adhesions between the epiglottis and tongue base, which were not clinically significant. A systematic review identified a total of six studies addressing the use of lingual tonsillectomy for persistent OSA after adenotonsillectomy, which was most common in children with hypotonia, craniofacial anomalies and obesity [110]. Rates of OSA resolution after lingual tonsillectomy ranged between 57 and 88 percent, although in three of the studies additional sites of obstruction were noted and supplemental surgical procedures were performed.

Genioglossus advancement combined with radiofrequency ablation of the tongue base was described in a group of 31 patients with persistent OSA after adenotonsillectomy, including 19 (61 percent) with Down syndrome [111]. Tongue base had been identified by cine MRI as the major site of collapse in 28 of 31 patients prior to surgery. The mean AHI improved from 14.1 to 6.4 events/hour, and mean nadir oxygen saturation increased from 87.4 to 90 percent (p <0.001 and 0.7 respectively). Success rate in curing OSA was 61 percent (defined as postoperative AHI <5 events/hour). Of note, some patients underwent concurrent surgical manipulations to address additional areas of collapse identified on imaging.

Submucosal minimally invasive lingual excision (SMILE) with a plasma-mediated radiofrequency device (coblation) under intraoral ultrasonic and endoscopic guidance was described in a small case series in children, with promising results [112]. A subsequent study in 96 adults compared SMILE with radiofrequency reduction of the tongue base, and demonstrated a significant reduction in the AHI for both groups [113]. Success rates were 64.6 and 41.7 percent, respectively, for the two procedures (defined as reduction of AHI by at least 50 percent and AHI <20), but the SMILE procedure was associated with increased morbidity and complications.

Expansion pharyngoplasty and lateral pharyngoplasty — In some children, OSA is associated with collapse of the lateral pharyngeal wall [97,98]. Surgical procedures to correct this problem include expansion sphincter pharyngoplasty (ESP) or lateral pharyngoplasty.

In ESP, the palatopharyngeus muscle in the lateral pharyngeal is rotated superiorly and laterally and sutured in place to create tension in the lateral wall. A complete or partial uvulectomy is then performed [114]. The outcomes of ESP were reported for a group of 25 children with severe OSA and lateral pharyngeal wall collapse identified on DISE who underwent modified ESP with adenotonsillectomy, and compared with 25 AHI-matched children who underwent adenotonsillectomy alone [115]. The AHI after surgery was lower in both groups. Cure (defined by AHI <1 event/hour) was seen in 64 percent of children in the group treated with modified ESP, compared with 8 percent in the group undergoing adenotonsillectomy alone (p <0.001), despite higher body mass index (BMI) and age in the ESP group.

Lateral pharyngoplasty (suturing of the tonsillar pillars) after adenotonsillectomy may also address lateral pharyngeal wall collapse and provide better control of OSA. In a prospective controlled study, 24 children with OSA alternately assigned to adenotonsillectomy with suturing of the tonsillar pillars (intervention group) or adenotonsillectomy alone (control group) [116]. The AHI improved by 79.9 percent in the intervention group, compared with 42.6 percent in the control group (p = 0.037). Success (defined by reduction of AHI of >50 percent) was seen in 91.6 percent of children in the intervention group, compared with 50 percent of children in the control group (p = 0.03). Complete resolution of OSA (defined by AHI <1) was seen in 50 percent of the children in the intervention group, compared with 16.7 percent in the control group (p = 0.097) [116].

Techniques to expand the lateral pharyngeal wall may therefore improve PSG measures of OSA compared with adenotonsillectomy alone in some children whose OSA arises in part from lateral pharyngeal wall collapse.

Supraglottoplasty — Supraglottoplasty is moderately effective for treating children with laryngomalacia and OSA. A systematic review examining studies of supraglottoplasty in children with persistent OSA after adenotonsillectomy identified four studies reporting on 77 children [110]. The pooled mean AHI improved from 12.1 events per hour to 4.4 events per hour after supraglottoplasty. Another systematic review and meta-analysis included 13 studies (three of which were also included the previously mentioned review) with a total of 138 pediatric patients [117]. In the subgroup of children with sleep-exclusive laryngomalacia, most of whom had prior adenotonsillectomy, AHI improved from pooled mean AHI of 14.0 to 3.3 events per hour, but only 10.5 percent had resolution of OSA, defined as an AHI <1. In the subgroup of children with congenital laryngomalacia, for whom the prior adenotonsillectomy status was not reported, the mean AHI improved from 20.4 to 4.0 events per hour, and oxygen saturation nadir also improved, while 26.5 percent had resolution of their OSA.

Mandibular distraction osteogenesis — Mandibular distraction osteogenesis had been used successfully to address severe OSA due to mandibular hypoplasia (micrognathia) in infants and children. The mandible is divided bilaterally and internal or external distraction devices are placed on each side. The distraction devices are then used to move the mandible forward at a rate of 1 to 2 mm/day until the desired advancement is achieved.

Outcomes of mandibular distraction osteogenesis were examined in a meta-analysis that included 74 articles with a total of 711 patients with a variety of craniofacial anomalies that were included in the analysis, including isolated and syndromic Pierre Robin sequence in 52.9 and 7 percent of children, respectively, and Treacher Collins syndrome in 6.8 percent of children [118]. Successful treatment of airway obstruction (defined as either tracheotomy avoidance or decannulation, avoidance of need for CPAP, or significant improvement or absence of OSA symptoms) was observed in 89.3 percent of children. Specifically, among the 181 patients with OSA, complete resolution or significant improvement in symptoms was reported in 95.6 percent of patients. Analysis was complicated by the fact that a variety of outcome measures were included and specific PSG values were not provided. Of note, a 23.8 percent complication rate was seen, most often in the form of infection, abscess, open bite deformity, nerve injuries, or hypertrophic scarring. The mean follow-up time was 28.7 months.

These data suggest that distraction osteogenesis can be considered as a treatment for severe OSA in selected patients with mandibular hypoplasia from congenital craniofacial defects, but the high complication rate mandates careful consideration when contemplating the procedure.

Uvulopharyngopalatoplasty — Uvulopalatopharyngoplasty (UPPP) is not widely used for the management of OSA in children, but has been successfully combined with adenotonsillectomy in small studies of children with neuromuscular disorders who are thought to be at high risk for persistent upper airway obstruction after adenotonsillectomy alone, including children with Down syndrome or other developmental delays [119-122]. Only one of these studies employed objective evaluation of improvement in OSA. In this study, 15 children with neurologic impairments and OSA were treated with UPPP in conjunction with adenotonsillectomy [122]. There was a statistically significant improvement in mean oxygen saturation nadir from 65 to 85 percent (p = 0.005). In long-term follow-up, 77 percent (10 of 13) of the patients did not require additional airway intervention. Small sample size, absence of control groups, and paucity of validated outcome measures preclude analysis of the utility of this procedure in the broader pediatric population. Potential complications include nasopharyngeal stenosis, palatal incompetence, and speech difficulties [123,124].  

Tracheotomy — Tracheotomy can be considered in children with persistent severe OSA despite surgical intervention, especially if they are intolerant of CPAP therapy. It can also be considered as a first-line treatment in children with severe OSA and airway obstruction who are not considered appropriate candidates for other surgical procedures. Although tracheotomy is an effective treatment for OSA and airway obstruction, it is associated with complications in as many as 43 to 77 percent of children, including bleeding, tracheoesophageal fistula, accidental decannulation, or tube occlusion [125,126].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Sleep-related breathing disorders including obstructive sleep apnea in children".)


Surgical removal of the tonsils and adenoids (adenotonsillectomy) is the first-line treatment of documented obstructive sleep apnea (OSA) or obstructive sleep-disordered breathing (SDB, without confirmation of OSA on polysomnography) in the general pediatric population. Complication rates are low and most studies indicate significant benefit, as measured by resolution or improvement in breathing during sleep (as measured by polysomnography), as well as in nighttime symptoms, daytime symptoms, and quality of life. (See 'Indications for surgery' above and 'Symptomatic outcomes' above.)

Higher risk – Risk factors for respiratory and other complications after adenotonsillectomy and for persistent disease after recovery include obesity (especially if severe), severe OSA at baseline, Down syndrome, craniofacial abnormalities, neuromuscular disorders, or mucopolysaccharidosis. Patients with sickle cell disease also are at risk for perioperative respiratory complications (table 1). For these patients, we recommend the following precautions:

Preoperative polysomnography (PSG) to assist in surgical decision-making. (See 'Polysomnography' above.)

Operative setting that permits tertiary care if needed, including observation in hospital or pediatric intensive care unit (PICU) after adenotonsillectomy. (See 'Referral to a tertiary care facility' above and 'Operative setting' above.)

Close clinical follow-up after adenotonsillectomy, with low threshold for performing postoperative PSG for many or all of these high-risk patients, especially if persistent symptoms are present. (See 'Indications for postoperative polysomnography' above.)

Standard risk – For patients without the above risk factors and who are otherwise healthy, adenotonsillectomy usually can be safely performed as an outpatient procedure. Expert opinion varies as to whether PSG should be routinely performed preoperatively for children with obstructive SDB, and whether young children (<3 years) should be routinely observed in-hospital overnight after the surgery. All patients should have a clinical reevaluation to determine whether snoring and other symptoms of SDB have resolved, and those with ongoing symptoms should have a postoperative PSG. (See 'Operative setting' above and 'Indications for postoperative polysomnography' above.)

A variety of surgical techniques have been developed for adenotonsillectomy. Traditionally, extracapsular (complete) tonsillectomy has been used, with either "hot" or "cold" dissection techniques. Intracapsular tonsillectomy (also known as partial tonsillectomy or tonsillotomy) is increasingly used. This technique in comparison to extracapsular tonsillectomy may permit more rapid recovery, but also may increase risk of tonsillar regrowth in some patients. The optimal surgical technique has not been established. (See 'Surgical techniques' above.)

For patients who have minimal adenotonsillar tissue, are poor candidates for adenotonsillectomy for any other reason, or who have persistent clinically significant OSA after adenotonsillectomy, treatment options may include continuous positive airway pressure (CPAP) or adjuvant surgical procedures, including uvulopalatopharyngoplasty, tongue base procedures, lateral and expansion pharyngoplasty, and mandibular distraction osteogenesis. These adjuvant surgical procedures are most commonly needed for patients with OSA risk factors other than adenotonsillar hypertrophy alone, such as in children with obesity, Down syndrome, craniofacial syndromes, or neuromuscular disease. Additional preoperative evaluation with techniques including drug-induced sleep endoscopy (DISE) or cine-magnetic resonance imaging can help to determine the site(s) of residual obstruction to assist operative planning. (See 'Adjuvant surgical procedures' above and 'Diagnostic procedures' above.)

Use of UpToDate is subject to the  Subscription and License Agreement.


  1. Ross RD, Daniels SR, Loggie JM, et al. Sleep apnea-associated hypertension and reversible left ventricular hypertrophy. J Pediatr 1987; 111:253.
  2. Kaemingk KL, Pasvogel AE, Goodwin JL, et al. Learning in children and sleep disordered breathing: findings of the Tucson Children's Assessment of Sleep Apnea (tuCASA) prospective cohort study. J Int Neuropsychol Soc 2003; 9:1016.
  3. Guilleminault C, Khramsov A, Stoohs RA, et al. Abnormal blood pressure in prepubertal children with sleep-disordered breathing. Pediatr Res 2004; 55:76.
  4. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2012; 130:576.
  5. Baugh RF, Archer SM, Mitchell RB, et al. Clinical practice guideline: tonsillectomy in children. Otolaryngol Head Neck Surg 2011; 144:S1.
  6. Cullen KA, Hall MJ, Golosinskiy A. Ambulatory surgery in the United States, 2006. Natl Health Stat Report 2009; :1.
  7. Weatherly RA, Mai EF, Ruzicka DL, Chervin RD. Identification and evaluation of obstructive sleep apnea prior to adenotonsillectomy in children: a survey of practice patterns. Sleep Med 2003; 4:297.
  8. Marcus CL, Moore RH, Rosen CL, et al. A randomized trial of adenotonsillectomy for childhood sleep apnea. N Engl J Med 2013; 368:2366.
  9. O'Brien LM, Mervis CB, Holbrook CR, et al. Neurobehavioral correlates of sleep-disordered breathing in children. J Sleep Res 2004; 13:165.
  10. Schlaud M, Urschitz MS, Urschitz-Duprat PM, Poets CF. The German study on sleep-disordered breathing in primary school children: epidemiological approach, representativeness of study sample, and preliminary screening results. Paediatr Perinat Epidemiol 2004; 18:431.
  11. Rosen CL, Larkin EK, Kirchner HL, et al. Prevalence and risk factors for sleep-disordered breathing in 8- to 11-year-old children: association with race and prematurity. J Pediatr 2003; 142:383.
  12. Kaditis AG, Finder J, Alexopoulos EI, et al. Sleep-disordered breathing in 3,680 Greek children. Pediatr Pulmonol 2004; 37:499.
  13. Lumeng JC, Chervin RD. Epidemiology of pediatric obstructive sleep apnea. Proc Am Thorac Soc 2008; 5:242.
  14. Li AM, So HK, Au CT, et al. Epidemiology of obstructive sleep apnoea syndrome in Chinese children: a two-phase community study. Thorax 2010; 65:991.
  15. Bixler EO, Vgontzas AN, Lin HM, et al. Sleep disordered breathing in children in a general population sample: prevalence and risk factors. Sleep 2009; 32:731.
  16. Katz ES, D'Ambrosio CM. Pediatric obstructive sleep apnea syndrome. Clin Chest Med 2010; 31:221.
  17. Shott SR, Amin R, Chini B, et al. Obstructive sleep apnea: Should all children with Down syndrome be tested? Arch Otolaryngol Head Neck Surg 2006; 132:432.
  18. Shintani T, Asakura K, Ishi K, et al. [Obstructive sleep apnea in children with cerebral palsy]. Nihon Jibiinkoka Gakkai Kaiho 1998; 101:266.
  19. Marcus CL, Keens TG, Bautista DB, et al. Obstructive sleep apnea in children with Down syndrome. Pediatrics 1991; 88:132.
  20. Dyken ME, Lin-Dyken DC, Poulton S, et al. Prospective polysomnographic analysis of obstructive sleep apnea in down syndrome. Arch Pediatr Adolesc Med 2003; 157:655.
  21. Daniel M, Bailey S, Walker K, et al. Airway, feeding and growth in infants with Robin sequence and sleep apnoea. Int J Pediatr Otorhinolaryngol 2013; 77:499.
  22. Afsharpaiman S, Sillence DO, Sheikhvatan M, et al. Respiratory events and obstructive sleep apnea in children with achondroplasia: investigation and treatment outcomes. Sleep Breath 2011; 15:755.
  23. Cielo CM, Taylor JA, Vossough A, et al. Evolution of Obstructive Sleep Apnea in Infants with Cleft Palate and Micrognathia. J Clin Sleep Med 2016; 12:979.
  24. Strauss T, Sin S, Marcus CL, et al. Upper airway lymphoid tissue size in children with sickle cell disease. Chest 2012; 142:94.
  25. Tran KD, Nguyen CD, Weedon J, Goldstein NA. Child behavior and quality of life in pediatric obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2005; 131:52.
  26. Tal A, Leiberman A, Margulis G, Sofer S. Ventricular dysfunction in children with obstructive sleep apnea: radionuclide assessment. Pediatr Pulmonol 1988; 4:139.
  27. Hodges S, Wailoo MP. Tonsillar enlargement and failure to thrive. Br Med J (Clin Res Ed) 1987; 295:541.
  28. Garetz SL. Behavior, cognition, and quality of life after adenotonsillectomy for pediatric sleep-disordered breathing: summary of the literature. Otolaryngol Head Neck Surg 2008; 138:S19.
  29. O'Brien LM, Mervis CB, Holbrook CR, et al. Neurobehavioral implications of habitual snoring in children. Pediatrics 2004; 114:44.
  30. Chervin RD, Ruzicka DL, Giordani BJ, et al. Sleep-disordered breathing, behavior, and cognition in children before and after adenotonsillectomy. Pediatrics 2006; 117:e769.
  31. Blunden S, Lushington K, Kennedy D, et al. Behavior and neurocognitive performance in children aged 5-10 years who snore compared to controls. J Clin Exp Neuropsychol 2000; 22:554.
  32. Brodsky L. Modern assessment of tonsils and adenoids. Pediatr Clin North Am 1989; 36:1551.
  33. Certal V, Catumbela E, Winck JC, et al. Clinical assessment of pediatric obstructive sleep apnea: a systematic review and meta-analysis. Laryngoscope 2012; 122:2105.
  34. Nolan J, Brietzke SE. Systematic review of pediatric tonsil size and polysomnogram-measured obstructive sleep apnea severity. Otolaryngol Head Neck Surg 2011; 144:844.
  35. Brietzke SE, Katz ES, Roberson DW. Can history and physical examination reliably diagnose pediatric obstructive sleep apnea/hypopnea syndrome? A systematic review of the literature. Otolaryngol Head Neck Surg 2004; 131:827.
  36. Chervin RD, Hedger K, Dillon JE, Pituch KJ. Pediatric sleep questionnaire (PSQ): validity and reliability of scales for sleep-disordered breathing, snoring, sleepiness, and behavioral problems. Sleep Med 2000; 1:21.
  37. Chervin RD, Weatherly RA, Garetz SL, et al. Pediatric sleep questionnaire: prediction of sleep apnea and outcomes. Arch Otolaryngol Head Neck Surg 2007; 133:216.
  38. Constantin E, Tewfik TL, Brouillette RT. Can the OSA-18 quality-of-life questionnaire detect obstructive sleep apnea in children? Pediatrics 2010; 125:e162.
  39. Goldstein NA, Stefanov DG, Graw-Panzer KD, et al. Validation of a clinical assessment score for pediatric sleep-disordered breathing. Laryngoscope 2012; 122:2096.
  40. Rosen CL, Wang R, Taylor HG, et al. Utility of symptoms to predict treatment outcomes in obstructive sleep apnea syndrome. Pediatrics 2015; 135:e662.
  41. Roland PS, Rosenfeld RM, Brooks LJ, et al. Clinical practice guideline: Polysomnography for sleep-disordered breathing prior to tonsillectomy in children. Otolaryngol Head Neck Surg 2011; 145:S1.
  42. Jambhekar S, Carroll JL. Diagnosis of pediatric obstructive sleep disordered breathing: beyond the gold standard. Expert Rev Respir Med 2008; 2:791.
  43. Mitchell RB, Pereira KD, Friedman NR. Sleep-disordered breathing in children: survey of current practice. Laryngoscope 2006; 116:956.
  44. Friedman NR, Perkins JN, McNair B, Mitchell RB. Current practice patterns for sleep-disordered breathing in children. Laryngoscope 2013; 123:1055.
  45. Marcus CL, Brooks LJ, Draper KA, et al. Diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2012; 130:e714.
  46. Thottam PJ, Choi S, Simons JP, Kitsko DJ. Effect of Adenotonsillectomy on Central and Obstructive Sleep Apnea in Children with Down Syndrome. Otolaryngol Head Neck Surg 2015; 153:644.
  47. Revenaugh PC, Chmielewski LJ, Edwards T, et al. Utility of preoperative cardiac evaluation in pediatric patients undergoing surgery for obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2011; 137:1269.
  48. Spencer DJ, Jones JE. Complications of adenotonsillectomy in patients younger than 3 years. Arch Otolaryngol Head Neck Surg 2012; 138:335.
  49. Walker P, Whitehead B, Rowley M. Role of paediatric intensive care following adenotonsillectomy for severe obstructive sleep apnoea: criteria for elective admission. J Laryngol Otol 2013; 127 Suppl 1:S26.
  50. Shine NP, Coates HL, Lannigan FJ, Duncan AW. Adenotonsillar surgery in morbidly obese children: routine elective admission of all patients to the intensive care unit is unnecessary. Anaesth Intensive Care 2006; 34:724.
  51. Dhiwakar M, Eng CY, Selvaraj S, McKerrow WS. Antibiotics to improve recovery following tonsillectomy: a systematic review. Otolaryngol Head Neck Surg 2006; 134:357.
  52. Pinder DK, Wilson H, Hilton MP. Dissection versus diathermy for tonsillectomy. Cochrane Database Syst Rev 2011; :CD002211.
  53. Tonsillectomy for Obstructive Sleep-Disordered Breathing or Recurrent Throat Infection in Children, Comparative Effectiveness Review Number 183, Agency for Healthcare Research and Quality. Available at: https://www.effectivehealthcare.ahrq.gov/ehc/products/620/2424/tonsillectomy-report-170113.pdf (Accessed on January 18, 2017).
  54. Koltai PJ, Solares CA, Mascha EJ, Xu M. Intracapsular partial tonsillectomy for tonsillar hypertrophy in children. Laryngoscope 2002; 112:17.
  55. Isaacson G. Pediatric intracapsular tonsillectomy with bipolar electrosurgical scissors. Ear Nose Throat J 2004; 83:702, 704.
  56. Friedman M, Wilson MN, Friedman J, et al. Intracapsular coblation tonsillectomy and adenoidectomy for the treatment of pediatric obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg 2009; 140:358.
  57. Wilson YL, Merer DM, Moscatello AL. Comparison of three common tonsillectomy techniques: a prospective randomized, double-blinded clinical study. Laryngoscope 2009; 119:162.
  58. Walton J, Ebner Y, Stewart MG, April MM. Systematic review of randomized controlled trials comparing intracapsular tonsillectomy with total tonsillectomy in a pediatric population. Arch Otolaryngol Head Neck Surg 2012; 138:243.
  59. Acevedo JL, Shah RK, Brietzke SE. Systematic review of complications of tonsillotomy versus tonsillectomy. Otolaryngol Head Neck Surg 2012; 146:871.
  60. Zagólski O. Why do palatine tonsils grow back after partial tonsillectomy in children? Eur Arch Otorhinolaryngol 2010; 267:1613.
  61. 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; 69:21.
  62. Celenk F, Bayazit YA, Yilmaz M, et al. Tonsillar regrowth following partial tonsillectomy with radiofrequency. Int J Pediatr Otorhinolaryngol 2008; 72:19.
  63. Borgström A, Nerfeldt P, Friberg D. Adenotonsillotomy Versus Adenotonsillectomy in Pediatric Obstructive Sleep Apnea: An RCT. Pediatrics 2017; 139.
  64. Walner DL, Parker NP, Miller RP. Past and present instrument use in pediatric adenotonsillectomy. Otolaryngol Head Neck Surg 2007; 137:49.
  65. Isaacson G. Pediatric tonsillectomy: an evidence-based approach. Otolaryngol Clin North Am 2014; 47:673.
  66. Klemetti S, Kinnunen I, Suominen T, et al. The effect of preoperative fasting on postoperative pain, nausea and vomiting in pediatric ambulatory tonsillectomy. Int J Pediatr Otorhinolaryngol 2009; 73:263.
  67. Windfuhr JP, Chen YS, Remmert S. Hemorrhage following tonsillectomy and adenoidectomy in 15,218 patients. Otolaryngol Head Neck Surg 2005; 132:281.
  68. De Luca Canto G, Pachêco-Pereira C, Aydinoz S, et al. Adenotonsillectomy Complications: A Meta-analysis. Pediatrics 2015; 136:702.
  69. Leong AC, Davis JP. Morbidity after adenotonsillectomy for paediatric obstructive sleep apnoea syndrome: waking up to a pragmatic approach. J Laryngol Otol 2007; 121:809.
  70. Brietzke SE, Gallagher D. The effectiveness of tonsillectomy and adenoidectomy in the treatment of pediatric obstructive sleep apnea/hypopnea syndrome: a meta-analysis. Otolaryngol Head Neck Surg 2006; 134:979.
  71. 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; 182:676.
  72. 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; 140:800.
  73. Venekamp RP, Hearne BJ, Chandrasekharan D, et al. Tonsillectomy or adenotonsillectomy versus non-surgical management for obstructive sleep-disordered breathing in children. Cochrane Database Syst Rev 2015; :CD011165.
  74. Garetz SL, Mitchell RB, Parker PD, et al. Quality of life and obstructive sleep apnea symptoms after pediatric adenotonsillectomy. Pediatrics 2015; 135:e477.
  75. Baldassari CM, Mitchell RB, Schubert C, Rudnick EF. Pediatric obstructive sleep apnea and quality of life: a meta-analysis. Otolaryngol Head Neck Surg 2008; 138:265.
  76. Montgomery-Downs HE, Crabtree VM, Gozal D. Cognition, sleep and respiration in at-risk children treated for obstructive sleep apnoea. Eur Respir J 2005; 25:336.
  77. Avior G, Fishman G, Leor A, et al. The effect of tonsillectomy and adenoidectomy on inattention and impulsivity as measured by the Test of Variables of Attention (TOVA) in children with obstructive sleep apnea syndrome. Otolaryngol Head Neck Surg 2004; 131:367.
  78. Goldstein NA, Fatima M, Campbell TF, Rosenfeld RM. Child behavior and quality of life before and after tonsillectomy and adenoidectomy. Arch Otolaryngol Head Neck Surg 2002; 128:770.
  79. Amin R, Anthony L, Somers V, et al. Growth velocity predicts recurrence of sleep-disordered breathing 1 year after adenotonsillectomy. Am J Respir Crit Care Med 2008; 177:654.
  80. Huang YS, Guilleminault C, Lee LA, et al. Treatment outcomes of adenotonsillectomy for children with obstructive sleep apnea: a prospective longitudinal study. Sleep 2014; 37:71.
  81. Ye J, Liu H, Zhang GH, et al. Outcome of adenotonsillectomy for obstructive sleep apnea syndrome in children. Ann Otol Rhinol Laryngol 2010; 119:506.
  82. Tauman R, Gulliver TE, Krishna J, et al. Persistence of obstructive sleep apnea syndrome in children after adenotonsillectomy. J Pediatr 2006; 149:803.
  83. Mitchell RB. Adenotonsillectomy for obstructive sleep apnea in children: outcome evaluated by pre- and postoperative polysomnography. Laryngoscope 2007; 117:1844.
  84. Costa DJ, Mitchell R. Adenotonsillectomy for obstructive sleep apnea in obese children: a meta-analysis. Otolaryngol Head Neck Surg 2009; 140:455.
  85. Shete MM, Stocks RM, Sebelik ME, Schoumacher RA. Effects of adeno-tonsillectomy on polysomnography patterns in Down syndrome children with obstructive sleep apnea: a comparative study with children without Down syndrome. Int J Pediatr Otorhinolaryngol 2010; 74:241.
  86. Gönüldaş B, Yılmaz T, Sivri HS, et al. Mucopolysaccharidosis: Otolaryngologic findings, obstructive sleep apnea and accumulation of glucosaminoglycans in lymphatic tissue of the upper airway. Int J Pediatr Otorhinolaryngol 2014; 78:944.
  87. Imanguli M, Ulualp SO. Risk factors for residual obstructive sleep apnea after adenotonsillectomy in children. Laryngoscope 2016; 126:2624.
  88. Zhang XM, Shi J, Meng GZ, et al. The effect of obstructive sleep apnea syndrome on growth and development in nonobese children: a parallel study of twins. J Pediatr 2015; 166:646.
  89. Lewis TL, Johnson RF, Choi J, Mitchell RB. Weight gain after adenotonsillectomy: a case control study. Otolaryngol Head Neck Surg 2015; 152:734.
  90. Katz ES, Moore RH, Rosen CL, et al. Growth after adenotonsillectomy for obstructive sleep apnea: an RCT. Pediatrics 2014; 134:282.
  91. Truong MT, Woo VG, Koltai PJ. Sleep endoscopy as a diagnostic tool in pediatric obstructive sleep apnea. Int J Pediatr Otorhinolaryngol 2012; 76:722.
  92. Durr ML, Meyer AK, Kezirian EJ, Rosbe KW. Drug-induced sleep endoscopy in persistent pediatric sleep-disordered breathing after adenotonsillectomy. Arch Otolaryngol Head Neck Surg 2012; 138:638.
  93. Wootten CT, Chinnadurai S, Goudy SL. Beyond adenotonsillectomy: outcomes of sleep endoscopy-directed treatments in pediatric obstructive sleep apnea. Int J Pediatr Otorhinolaryngol 2014; 78:1158.
  94. Boudewyns A, Verhulst S, Maris M, et al. Drug-induced sedation endoscopy in pediatric obstructive sleep apnea syndrome. Sleep Med 2014; 15:1526.
  95. Chan DK, Liming BJ, Horn DL, Parikh SR. A new scoring system for upper airway pediatric sleep endoscopy. JAMA Otolaryngol Head Neck Surg 2014; 140:595.
  96. Lam DJ, Weaver EM, Macarthur CJ, et al. Assessment of pediatric obstructive sleep apnea using a drug-induced sleep endoscopy rating scale. Laryngoscope 2016; 126:1492.
  97. Ulualp SO, Szmuk P. Drug-induced sleep endoscopy for upper airway evaluation in children with obstructive sleep apnea. Laryngoscope 2013; 123:292.
  98. Shott SR, Donnelly LF. Cine magnetic resonance imaging: evaluation of persistent airway obstruction after tonsil and adenoidectomy in children with Down syndrome. Laryngoscope 2004; 114:1724.
  99. Donnelly LF, Shott SR, LaRose CR, et al. Causes of persistent obstructive sleep apnea despite previous tonsillectomy and adenoidectomy in children with down syndrome as depicted on static and dynamic cine MRI. AJR Am J Roentgenol 2004; 183:175.
  100. Peppard PE, Young T, Palta M, et al. Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000; 284:3015.
  101. Verhulst SL, Franckx H, Van Gaal L, et al. The effect of weight loss on sleep-disordered breathing in obese teenagers. Obesity (Silver Spring) 2009; 17:1178.
  102. Kalra M, Inge T, Garcia V, et al. Obstructive sleep apnea in extremely overweight adolescents undergoing bariatric surgery. Obes Res 2005; 13:1175.
  103. Brouillette RT, Manoukian JJ, Ducharme FM, et al. Efficacy of fluticasone nasal spray for pediatric obstructive sleep apnea. J Pediatr 2001; 138:838.
  104. Kheirandish-Gozal L, Gozal D. Intranasal budesonide treatment for children with mild obstructive sleep apnea syndrome. Pediatrics 2008; 122:e149.
  105. Chadha NK, Zhang L, Mendoza-Sassi RA, César JA. Using nasal steroids to treat nasal obstruction caused by adenoid hypertrophy: does it work? Otolaryngol Head Neck Surg 2009; 140:139.
  106. Kheirandish L, Goldbart AD, Gozal D. Intranasal steroids and oral leukotriene modifier therapy in residual sleep-disordered breathing after tonsillectomy and adenoidectomy in children. Pediatrics 2006; 117:e61.
  107. Friedman O, Chidekel A, Lawless ST, Cook SP. Postoperative bilevel positive airway pressure ventilation after tonsillectomy and adenoidectomy in children--a preliminary report. Int J Pediatr Otorhinolaryngol 1999; 51:177.
  108. Fujita S, Woodson BT, Clark JL, Wittig R. Laser midline glossectomy as a treatment for obstructive sleep apnea. Laryngoscope 1991; 101:805.
  109. Lin AC, Koltai PJ. Persistent pediatric obstructive sleep apnea and lingual tonsillectomy. Otolaryngol Head Neck Surg 2009; 141:81.
  110. Manickam PV, Shott SR, Boss EF, et al. Systematic review of site of obstruction identification and non-CPAP treatment options for children with persistent pediatric obstructive sleep apnea. Laryngoscope 2016; 126:491.
  111. Wootten CT, Shott SR. Evolving therapies to treat retroglossal and base-of-tongue obstruction in pediatric obstructive sleep apnea. Arch Otolaryngol Head Neck Surg 2010; 136:983.
  112. Maturo SC, Mair EA. Submucosal minimally invasive lingual excision: an effective, novel surgery for pediatric tongue base reduction. Ann Otol Rhinol Laryngol 2006; 115:624.
  113. Friedman M, Soans R, Gurpinar B, et al. Evaluation of submucosal minimally invasive lingual excision technique for treatment of obstructive sleep apnea/hypopnea syndrome. Otolaryngol Head Neck Surg 2008; 139:378.
  114. Pang KP, Woodson BT. Expansion sphincter pharyngoplasty: a new technique for the treatment of obstructive sleep apnea. Otolaryngol Head Neck Surg 2007; 137:110.
  115. Ulualp SO. Modified expansion sphincter pharyngoplasty for treatment of children with obstructive sleep apnea. JAMA Otolaryngol Head Neck Surg 2014; 140:817.
  116. Chiu PH, Ramar K, Chen KC, et al. Can pillar suturing promote efficacy of adenotonsillectomy for pediatric OSAS? A prospective randomized controlled trial. Laryngoscope 2013; 123:2573.
  117. Camacho M, Dunn B, Torre C, et al. Supraglottoplasty for laryngomalacia with obstructive sleep apnea: A systematic review and meta-analysis. Laryngoscope 2016; 126:1246.
  118. Tahiri Y, Viezel-Mathieu A, Aldekhayel S, et al. The effectiveness of mandibular distraction in improving airway obstruction in the pediatric population. Plast Reconstr Surg 2014; 133:352e.
  119. Strome M. Obstructive sleep apnea in Down syndrome children: a surgical approach. Laryngoscope 1986; 96:1340.
  120. Seid AB, Martin PJ, Pransky SM, Kearns DB. Surgical therapy of obstructive sleep apnea in children with severe mental insufficiency. Laryngoscope 1990; 100:507.
  121. Kosko JR, Derkay CS. Uvulopalatopharyngoplasty: treatment of obstructive sleep apnea in neurologically impaired pediatric patients. Int J Pediatr Otorhinolaryngol 1995; 32:241.
  122. Kerschner JE, Lynch JB, Kleiner H, et al. Uvulopalatopharyngoplasty with tonsillectomy and adenoidectomy as a treatment for obstructive sleep apnea in neurologically impaired children. Int J Pediatr Otorhinolaryngol 2002; 62:229.
  123. Fairbanks DN. Uvulopalatopharyngoplasty complications and avoidance strategies. Otolaryngol Head Neck Surg 1990; 102:239.
  124. Carenfelt C, Haraldsson PO. Frequency of complications after uvulopalatopharyngoplasty. Lancet 1993; 341:437.
  125. Mahadevan M, Barber C, Salkeld L, et al. Pediatric tracheotomy: 17 year review. Int J Pediatr Otorhinolaryngol 2007; 71:1829.
  126. Carr MM, Poje CP, Kingston L, et al. Complications in pediatric tracheostomies. Laryngoscope 2001; 111:1925.
Topic 97855 Version 12.0

Topic Outline



All topics are updated as new information becomes available. Our peer review process typically takes one to six weeks depending on the issue.