Stacey L. Ishman and Christopher R. Roxbury
Sleep disordered breathing (SDB) is now well recognized as a common condition in children, representing a spectrum ranging from simple snoring to upper airway resistance syndrome (UARS) to obstructive sleep apnea syndrome (OSAS). Children with obesity, Down syndrome, and craniofacial abnormalities are at high risk for SDB. While adults with SDB commonly present with excessive daytime sleepiness, daytime signs and symptoms are less apparent in affected children. More commonly, caregivers report signs of SDB such as snoring, gasping for breath at night, and poor school performance.
While milder forms of SDB are not generally associated with airflow restriction or oxygen desaturation, OSAS is characterized by apneas, hypopneas, and respiratory effort-related arousals (RERAs). Severe OSAS in children can lead to cardiovascular and pulmonary complications. SDB, even of milder severity such as primary snoring, has been associated with behavioral and neurocognitive disturbances, decreased school performance, and quality of life impairment. As such, it is important to recognize these entities early and implement proper medical and/or surgical therapy.
Unfortunately, diagnosis of pediatric SDB is not as straightforward as it is in adult patients. A standardized approach to clinical diagnosis and universal clinical screening protocols is lacking. Clinicians must have a high index of suspicion, especially in high-risk children.
A thorough history is the cornerstone of diagnosis of SDB in children. In general, children with OSAS display similar stereotypical nighttime symptoms as adults with OSAS. These include snoring, gasping for breath, increased respiratory effort, abnormal movements during sleep, witnessed apneas, and restless sleep with or without frequent awakenings. Children may also display several nonspecific daytime symptoms, including mouth breathing, hyponasality, and dysphagia, as well as psychological and behavioral changes including hyperactivity, increased aggression, and poor performance in school. Enuresis is also associated with pediatric SDB. Daytime sleepiness is not a common complaint in affected children.
In an attempt to emphasize early diagnosis and treatment, the American Academy of Pediatrics in 2002 recommended universal screening of children for snoring during routine pediatric care.1 However, over 9% of the general pediatric population may suffer from habitual snoring, which may occur in the absence of frank OSAS. Moreover, studies have shown that the caregiver's description of the symptoms is not an accurate means to diagnose OSAS.2History and physical examination findings correlate poorly with polysomnographic findings.
The clinician must fully evaluate genetic conditions that predispose to oropharyngeal or nasopharyngeal obstruction, creating increased risk for OSAS. Such conditions include Down, Crouzon, and Apert syndromes as well as bilateral choanal atresia. Furthermore, syndromes with retrognathia or micrognathia such as Pierre Robin sequence and Treacher Collins syndrome have been associated with SDB. Finally, conditions that affect tone in the pharynx and upper airway, such as cerebral palsy, can predispose to OSAS that is quite difficult to treat.
Epidemiologic studies have shown that the overall prevalence of pediatric OSAS ranges from 1 to 4%. While it has been thought that prevalence is equal between male and female children, a 2008 systematic review of the literature found that males are more likely to suffer from SDB than females.3 The incidence is also higher in African Americans than in Caucasians. Finally, obesity has also been associated with an increased incidence of SDB in children and adults (Table 7.1).
The age of a child at presentation is a key consideration when evaluating for SDB, as neonates and infants may have different signs, symptoms, and causes of SDB than older children. Evaluation of a child with possible SDB should begin with an assessment of growth and weight gain. While infants and young children may be more likely to present with poor weight gain or failure to thrive, older children with obstructive sleep apnea (OSA) are more likely to be overweight or obese.
A thorough head and neck examination should be performed to search for the site of airway obstruction. Any signs of syndromes affecting craniofacial anatomy or airway tone should be noted. In addition, the nasal cavity should be examined for inflammation, swelling, or masses, and the posterior nasal cavity should be inspected for choanal stenosis or atresia when suspected. A thorough examination of the nasopharynx may also include an assessment of the adenoid size using nasopharyngoscopy or radiographs.
The oral cavity and oropharynx must also be examined, inspecting for macroglossia as well as palpating the hard and soft palate to assess for overt or submucous cleft palate. Tonsillar size is assessed by grading on a 4-point scale with a 0 for tonsils that have been previously removed, 1+ for tonsils within the tonsillar pillars, 2+ for tonsils that protrude just beyond the pillars, 3+ for tonsils that protrude greater than 50% of the way to the midline, and 4+ for tonsils that meet in the midline (Fig. 7.1).
Table 7.1 Relevant Pediatric Obstructive Sleep Apnea History and Physical Examination
• Gasping for breath or choking during sleep
• Increased respiratory effort
• Witnessed apneas
• Restless sleep with or without frequent awakenings
• Nocturnal enuresis (secondary)
• Mouth breathing
• Aggressive behavior or hyperactivity
• Poor school performance
• Excessive daytime sleepiness (less common than in adults)
• Blood pressure, height and weight with body mass index
• Obesity or failure to thrive
• Craniofacial alignment—mandible and maxilla position/size
• Adenoid facies
• External nasal deformity
• Nasal valve (internal and external)
• Inferior turbinates
• Rhinorrhea and nasal edema
• Tonsil size and position (i.e., glossoptosis)
• Modified Mallampati score
• Palate and uvula position
• Dentition and oropharyngeal crowding
• Relative position of the hyoid
• Cardiovascular examination
• Chest wall deformity
• Craniofacial or syndromic abnormalities
A recent systematic review has shown that the association between tonsillar size and obstruction as quantified by polysomnography (PSG) may not be as strong as once suspected.4 In this study, 20 articles (mean n = 161) were analyzed with 11 supporting a correlation between tonsillar size and obstruction and 9 showing no association. It was the higher quality studies that showed no correlation between tonsil size and OSAS severity. While tonsillar size may be used as a clinical guide, providers must be aware that size may not be the best predictor of OSAS.
Figure 7.1 Tonsil grading.
Reprinted with permission from: John Wiley and Sons. Friedman M, Ibrahim H, Joseph N. Staging of obstructive sleep apnea/hypopnea syndrome: a guide to appropriate treatment. The Laryngoscope 2004;114(3):454–459.
As OSAS has been associated with high body mass index (BMI) score and adenotonsillar hypertrophy in some studies, some clinicians may proceed directly to adenotonsillectomy (AT) in healthy children with signs of SDB and enlarged tonsils on physical examination. However, PSG is considered the gold standard test for diagnosis of OSAS in children.
Commonly referred to as the “sleep study,” PSG is the simultaneous electrographic recording of multiple variables during sleep. These parameters include sleep stage, snoring, airflow, respiratory effort, gas exchange, limb position, and limb movement (Fig. 7.2A–C). PSG can help distinguish OSAS from other disorders such as primary snoring, narcolepsy, nocturnal seizures, periodic limb movements, and restless leg syndrome. PSG also allows clinicians to stratify the severity of OSAS, and may in fact help identify the children at increased risk for respiratory compromise postoperatively who would benefit from hospital admission.
Unfortunately, there are no validated severity scales for diagnosing mild, moderate, and severe OSAS in children. The current standard research definition recognizes a respiratory disturbance index (RDI) of 1 to <5 events per hour to be mild OSAS, 5 to <10 events per hour as moderate OSAS, and 10 or more events per hour as severe OSAS. However, others have advocated that normal breathing may occur up to an apnea–hypopnea index (AHI) of two obstructive events per hour.5 It is important to note, however, that there are significant differences in the criteria for the performance, scoring, and interpretation of pediatric and adult PSG. As such, it is important that these laboratories have experience in the performance and interpretation of PSG studies in children to obtain accurate and reliable results.
Figure 7.2 (A) Obstructive apnea with cessation of airflow associated with continued respiratory effort; (B) hypopnea with decreased nasal airflow and desaturation; and (C) respiratory event-related arousal with decreased nasal airflow with an arousal.
A recent review paper has challenged the necessity of PSG for the diagnosis of pediatric OSA.6 Best practice guidelines proposed by this paper suggest that AT may be performed without PSG in otherwise healthy children with a history consistent with symptoms of SDB and physical examination findings of adenotonsillar hypertrophy. In addition, they propose that preoperative PSG is only needed in children <3 years of age, or when adenotonsillar size is discordant with the degree of airway obstruction.
Due to the difficulties in access to and performance of overnight PSG in children, portable, or “in-home,” monitoring devices have been suggested for the diagnosis of pediatric SDB. The American Academy of Sleep Medicine (AASM) updated its guidelines in 2007 to recommend that such in-home studies include measures of airflow, blood oxygenation, and respiratory effort at a minimum. However, in-home testing has not been validated in children.
In 2011, the American Academy of Otolaryngology-Head and Neck Surgery (AAO-HNS) published a clinical practice guideline on use of PSG before tonsillectomy for SDB in children.7 These guidelines suggest referral for PSG before tonsillectomy for children with high risk factors such as obesity, Down syndrome, craniofacial abnormalities, neuromuscular disorders, sickle cell disease, or mucopolysaccharidoses (MPS). PSG for otherwise healthy children is recommended if the need for surgery is uncertain or if there is a discrepancy between adenoid/tonsil size and SDB symptoms.
In addition, the AAO-HNS advocates communication of PSG results to the anesthesiologist before induction of anesthesia, as the results of PSG can help guide intraoperative decision-making and anesthesia management, and can affect postoperative care plans. For instance, the guidelines suggest postoperative admission for children under the age of 3 or with severe OSAS as defined by an AHI ≥10 or an oxygen saturation nadir <80%. Young age and OSAS severity correlate well with respiratory compromise after adenotonsillectomy that may require intervention.5
Finally, the AAO-HNS suggests obtaining in-laboratory 16 channel PSG for children rather than portable monitoring, as the aforementioned AASM guidelines for in-home testing are based on use in adults. PSG for children may be expensive, inconvenient, and unavailable, and is an imperfect gold standard. As such, there has been a search for simpler ways to clinically screen for OSAS such as the OSA-18 quality of life questionnaire, Pediatric Sleep Questionnaire and the Brouillette OSA score. However, each of these has been shown to have poor specificity for OSAS diagnosis.
Childhood obesity, with its rapidly increasing prevalence, is perhaps the most important risk factor for the development of pediatric SDB. In 2007, 16.4% of U.S. children were obese and 31.6% were overweight. As many of these children will be asymptomatic, and are later found to have moderate or even severe OSAS by PSG, routine PSG testing is particularly important for obese children.
A recent review of children undergoing ambulatory surgery at a university medical center found that 36% of obese patients presented for otolaryngologic procedures, most commonly AT, supporting the observation that obesity increases the propensity for airway obstruction.8 Proposed mechanisms for this include the presence of excess adipose tissue in the upper airway causing distortion and collapse, and neuromotor dysfunction during sleep. Unfortunately, recent studies have shown that 49 to 88% of obese children will have obstructive symptoms even after surgery.1
OSAS is also more common in Down syndrome, where as many as 31 to 63% of children may suffer from OSAS.7 Features of Down syndrome that increase the risk of OSAS are a large tongue, midface hypoplasia, a stocky body habitus, and hypertrophy of not only the adenoids and palatine tonsils but also the lingual tonsils. A recent study showed that 80% of Down syndrome patients in the age group of 4 to 63 months had abnormal PSG results, and caregiver assessments using the Children's Sleep Habits Questionnaire did not predict these abnormalities.9 Based on these results, it was recommended that all children with Down syndrome be screened for OSAS with a baseline PSG, preferably performed between the ages of 3 and 5. In addition, the American Academy of Pediatrics recommended in 2001 that parents of young children with Down syndrome children be questioned about SDB.
Adenotonsillectomy rarely cures OSAS in children with Down syndrome. A recent study suggests that up to 75% of Down syndrome patients will have an abnormal PSG after surgery. It has been suggested that persistent OSAS is likely from additional areas of anatomic airway obstruction and abnormal neuromotor tone common to these children. A recent study of children less than 2 years old with Down syndrome suggests that some will outgrow their OSAS. In this study, 16 of the 29 patients studied had OSAS, of which 6 were started on continuous positive airway pressure (CPAP) only. Of these, 3 children (50% of the CPAP population and 19% of the total study population) were found to have no evidence of OSAS on follow-up PSG within the next 10 months.10 Such resolution has been seen in other young children without Down syndrome.
Other genetic syndromes that predispose children to SDB are the MPS, such as Hunter and Hurler syndromes (Table 7.2). Presumably, stereotypic anatomic changes in this patient population such as a short neck, high epiglottis, deep cervical fossa, large tongue, adenotonsillar hypertrophy, and a hypoplastic mandible all contribute to this predisposition toward OSA. Progressive deposition of glycosaminoglycans in the airways contributes to obstruction as well. OSAS has been seen in up to 64% of these patients.11
Children with craniosynostosis, as seen in Pfeiffer, Apert, and Crouzon syndromes have SDB in up to 53% of cases. While AT may help those patients with mild craniofacial deformity, OSAS refractory to AT in this group often requires tracheostomy or long-term CPAP. Midface advancement is also a reasonable alternative, with critical objective assessment after surgery. Alternatively, a retrospective analysis of long-term nasopharyngeal airway use in children with a mean age of 5.8 ± 4.1 years showed a significant improvement in oxygen saturations when monitored by PSG.12
Obstructive sleep apnea is also more common in children with cleft lip and palate, presumably due to midface hypoplasia and retrognathia, which lead to a narrowed upper airway that may persist even after surgery. In a recent review of 459 patients with nonsyndromic cleft palate/lip, 37.5% had symptoms of SDB while 8.5% had OSAS diagnosed by PSG.13
Achondroplasia patients are also at increased risk of OSAS due to characteristic craniofacial anatomy that involves midface hypoplasia, skull enlargement with narrowing of the skull base, and stenosis of the nasal and nasopharyngeal airways. These patients may also experience mixed and central apnea due to brainstem compression secondary to a narrowed foramen magnum. A recent retrospective chart review of children ages 3 to 14 with achondroplasia showed a SDB prevalence of 54.3%.14 AT was shown to improve symptoms in the majority of patients as measured by AHI, but 5.3 to 12.3% of patients required some additional form of therapy.
Table 7.2 Conditions Associated with Increased Risk of Sleep Disordered Breathing in Children
• Apert syndrome
• Beckwith-Wiedeman syndrome
• Cerebral palsy
• Choanal stenosis or atresia
• Cleft lip/palate
• Crouzon syndrome
• Down syndrome
• Goldenhar syndrome/hemifacial microsomia
• Klippel-Feil syndrome
• Pfieffer syndrome
• Pierre Robin sequence
• Pfeiffer syndrome
• Pharyngeal flap surgery
• Prader-Willi syndrome
• Recurrent respiratory papillomatosis (oropharyngeal)
• Sickle cell disease
• Treacher Collins syndrome
Neuromuscular disorders such as cerebral palsy, muscular dystrophies, as well as spinal muscular atrophy are frequently associated with SDB and OSAS due to hypotonia of the pharyngeal musculature. In one review, 31% of patients with Duchenne muscular dystrophy (DMD) had OSAS diagnosed by PSG when referred for such testing.15 DMD patients should undergo annual PSG from the time they are wheelchair-bound or when signs of OSAS are seen.
Children with cerebral palsy frequently have OSAS due to decreased neuromuscular control. These children may also have difficulty compensating for airway obstruction during sleep due to a decreased ability to reposition themselves. Unfortunately, these children are also less likely to respond to AT, and are more likely to require additional pharyngeal surgery, CPAP, or even tracheotomy in almost 14% of cases.16
Dental Appliances and Rapid Maxillary Expansion
In children with OSAS and malocclusion rapid maxillary expansion (RME) can be considered, especially if AT is not indicated or desired by the caregivers or who have persistent symptoms after AT. Fourteen children who underwent RME were found to have reduced snoring as well as a substantial reduction in the AHI.17 While this report found sustained cure after 24 months, follow-up was not available for all patients, and treatment failures were seen in patients with tonsillar enlargement and/or overweight. Dental appliances are another nonsurgical option for OSAS treatment. The goal of this therapy is to stabilize and increase the oropharyngeal and hypopharyngeal airway spaces. There is limited data to support the use of such appliances in children. In a case− control study, children with mild to moderate OSAS were more likely to have a reduced mandibular length, overbite, and smaller dental arch, in addition to a more superiorly located hyoid bone than healthy controls. In one study, 20 children with OSAS were treated daily with a dental appliance for 6 months showed a mean decrease in the RDI from 7.9 ± 1.8 pretreatment to 3.7 ± 6.8 posttreatment (p<0.001).18 Dental appliances may be efficacious in children, but more data are needed to support this.
A 2005 Cochrane review identified two randomized controlled trials of intranasal steroids for children with OSAS.19 Both studies showed a small but statistically significant decrease in the mean AHI in the treatment group, but cure was not seen in most patients. Leukotriene modifiers have also been studied, with one study of children with mild OSAS showing that a 16-week course of monteleukast improved AHI (pretreatment mean 3.0 ± 0.22, posttreatment mean 2.0 ± 0.3, p = 0.017) and hypercarbia as well as reducing adenoid size.20
Figure 7.3 Forest plot for success in achieving an apnea–hypopnea index >5 postoperatively.
Source: Friedman M, Wilson MN, 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, Figure 3.
Since 2006, nasal CPAP has been approved for use in children older than 7 or weighing more than 40 pounds. As of 2005, there have been at least 2 masks approved by the U.S. Food and Drug Administration for use in children 2 years and older, but there are still none approved for children younger than 2. In addition to problems with mask fit, the masks are often uncomfortable, and compliance is poor (Fig. 7.3). A recent analysis of effectiveness and compliance in children 2 to 16 years old found that CPAP reduced RDI and increased oxygen saturation, but 30% of the subjects discontinued the treatment within 6 months.21 Complications of CPAP include dermatitis, nasal obstruction, and nasal dryness. In a study of children 6 months to 18 years of age using CPAP, 48% had skin injury with erythema and skin necrosis, 68% had global facial flattening, and 37% were found to have maxillary retrusion.22
The inability of children to tolerate CPAP has lead researchers to seek other ways to deliver air to these children in a manner that might be more tolerable. One such study showed that children treated with transnasal insufflation (TNI), warm humidified air delivered through a nasal cannula, have reductions in AHI comparable to those treated with CPAP.23 This method was trialed in 12 children ages 7 to 14, with OSA symptoms ranging from mild to severe. All children received high flow oxygen through a nasal cannula at 20L/min, and had improved oxygen stores and decreased arousals, which decreased the AHI from a baseline mean of 11 +/− 3 to 5 +/− 2 events per hour (p<0.01), comparable to that on CPAP in the majority of children. While further evidence is required, it may prove to be an appealing noninvasive alternative in children.
Two studies of adenoidectomy alone for childhood SDB show limited benefits. The first reported on 206 patients followed for 3 to 5 years after adenoidectomy performed for nasal obstruction in 89%, snoring in 88%, and obstructed breathing in 44% of the subjects.24 Results of this study indicated that 80% of children had an improvement in symptoms postoperatively, but that symptomatic re-growth of the adenoids may occur in as many as 3% of patients. The second study analyzes the incidence of future tonsillectomy or revision adenoidectomy in 48 children who underwent adenoidectomy for obstructive symptoms compared with 52 who had adenoidectomy for nonobstructive reasons.25 In this study, 38% of children with obstructive symptoms underwent subsequent surgery versus only 19% of those with nonobstructive symptoms. While both of these studies suggest that adenoidectomy alone improves OSA in children, they do not provide a comparison to AT. Additionally, re-growth of adenoids can occur, especially in children who have their adenoids removed before 6 years of age. This results in recurrence of obstructive symptoms and need for revision adenoidectomy.
OSAS is the most common indication for AT in the United States. Early complications include bleeding, vomiting, and dehydration due to increased pain on swallowing and poor oral intake. Late complications, which generally occur within 1 week of the procedure, include delayed bleeding, velopharyngeal insufficiency (VPI), and nasopharyngeal stenosis (NPS). Preoperative evaluation should include assessment of bleeding risk, evaluation of clinical factors associated with postoperative respiratory difficulties, and determination of risk for postoperative hypernasality.
AT has been shown to lead to a complete resolution in symptoms in up to 71% of patients. Multiple studies have shown that the procedure improves quality of life, neuro-cognitive, and behavioral measures. However, recent evidence suggests that more children are not completely cured of OSAS by AT than previously suspected. A recent review of 578 children who had AT for OSAS showed that 90.1% had an improved AHI, with a mean of 18.2 ± 21.4 preoperatively to 4.1 ± 6.4 postoperatively. Only 27.2% of children had a complete cure of OSAS as defined by an AHI <1 event per hour, while 21.6% had postoperative AHI >5 events per hour.26 In light of these findings, parents must be counseled that AT may not completely cure the child's obstructive symptoms (Fig. 7.4).
Tonsillectomy versus Tonsillotomy
Partial tonsillectomy, intracapsular tonsillectomy, or tonsillotomy has been advocated as a less-morbid alternative to total tonsillectomy, as it reduces tonsillar bulk while preserving the tonsillar capsule and preventing exposure of the pharyngeal musculature. Advocates suggest that tonsillotomy leads to decreased pain and postoperative morbidity than traditional total tonsillectomy, with similar outcomes in terms of snoring and recurrent infections.
In one study, microdebrider intracapsular tonsillectomy was shown to result in efficient removal of tonsil tissue, fewer complications and less pain, in addition to a quicker return to normal diet and activity.27Quality of life measures have also been found to improve after tonsillectomy and tonsillotomy.
Figure 7.4 Adherence of CPAP in children shows 30% stopped using CPAP before 6 months.
Source: Marcus CL, Rosen G, Ward SL, et al. Adherence to and effectiveness of positive airway pressure therapy in children with obstructive sleep apnea. Pediatrics 2006;117(3):e442–e451, Figure 2a.
BPAP, bilevel positive airway pressure; CPAP, continuous positive airway pressure.
Most studies comparing tonsillotomy to tonsillectomy only measure outcomes such as postoperative pain, time to return to normal diet and activity, and quality of life. One retrospective study of 33 patients who underwent tonsillotomy and 16 who underwent tonsillectomy compared the procedures in terms of snoring, tonsillar regrowth, recurrent tonsillitis, and recurrent obstruction, and found no statistically significant differences between the two groups.28
Nasal obstruction is a known risk factor for sleep-disordered breathing. Nasal obstruction in children can either cause or exacerbate symptoms of OSAS, likely from turbinate hypertrophy. A randomized controlled trial of radiofrequency inferior turbinate ablation showed improved nasal obstruction and increased nasal CPAP compliance.29 However, turbinate reduction in children remains controversial, as many children with turbinate hypertrophy have benefitted from adenoidectomy alone.
Some children with complex causes of OSAS, especially those with neurological impairment and craniofacial syndromes, may benefit from UPPP as this procedure addresses posterior oropharyngeal obstruction by the soft palate and lateral pharyngeal walls. However, these studies are limited and subject to selection bias. Most studies of UPPP have been performed in adults, with reported success rates of 30 to 65% when performed alone. Regardless of the technique, the surgeon must be meticulous in both patient selection and technical aspects of surgery to avoid complications such as VPI and NPS.
While lingual tonsil hypertrophy is uncommon in children, growing evidence suggests that children with Down syndrome and obesity are at increased risk for enlargement of the lingual tonsils.30 In addition, cases of airway obstruction that resolved after lingual tonsillectomy alone have been reported. A recent series described 26 patients (age range, 3 to 20 years) with persistent OSAS after tonsillectomy who were treated with endoscopic-assisted lingual tonsillectomy. These patients were improved but not cured after this surgery, with reduction of mean RDI from 14.7 to 8.1 after surgery. Lingual tonsillectomy should be performed with caution to avoid pharyngeal scarring. A recent study of lingual tonsillectomy performed as part of multilevel upper airway surgery showed that 8.2% of children developed oropharyngeal stenosis (OPS).31 Thus, a more conservative, multistep approach may be necessary in children requiring multilevel surgery if they require lingual tonsillectomy.
Tongue Reduction Techniques
Radiofrequency ablation of the tongue base has been shown in adult populations to have moderate ability to improve ESS and RDI with minimal complications. However, this technique has been reported in children only to treat lymphatic and vascular malformations of the tongue.
Other Methods to Address Retroglossal Obstruction
Experience is at best limited for additional procedures that focus on the base of the tongue in children with complex OSAS. Case reports have found decreases in OSAS when children with macroglossia and tongue base hypertrophy were treated with a tongue suspension suture. Tongue reductions can also help treat OSAS in children with macroglossia such as those with Beckwith-Wiedemann syndrome and lymphovascular malformations
Hyoid suspension has also been used to treat obstruction stemming from the base of the tongue although there is very little published pediatric data. Genioglossal advancement (GGA) has been studied in children with OSAS. Adult studies of GGA have shown up to a 70% decrease in RDI, but this procedure was almost always performed simultaneously with other upper airway procedures such as UPPP. A retrospective study of GGA was also performed to determine which patients are likely to benefit most from this procedure. In this study, 28 patients in the age group of 3 to 22 years who had previously undergone GGA to treat OSA were assessed by postoperative PSG. Of them, 17 (61%) were considered successful and 11 (39%) were considered to have failed.32 Subsequently, the authors analyzed static and dynamic cine MR studies and determined that only relative tongue size and small adenoid size predicted success with GGA.
Children with craniofacial abnormalities may benefit from specific procedures to correct these anatomical deformities. Children with midface hypoplasia may undergo Le Fort osteotomies or midface advancement. Of course, patients must undergo a thorough evaluation of craniofacial anatomy and neuromotor status to determine candidacy for such procedures.
Tracheostomy is a definitive treatment for OSAS, as it by definition bypasses virtually all contributing sites of upper airway obstruction. However, high morbidity and complex care issues relegate the role of tracheotomy to treatment of children with complex causes of OSAS that have not responded to more conservative surgical and nonsurgical treatments. It may also be useful in patients with neurologic deficits who have difficulty protecting their own airway, as well as an adjunct procedure before or during craniofacial surgery.
AT is one of the most common procedures performed today, and children with SDB are at high risk for complications. AAO-HNS guidelines suggest overnight admission after AT in children less than three years old, and for those with severe OSA (AHI >10, O2 nadir <80%), as these children are at highest risk for postoperative airway compromise. In addition, admission should be considered in children with more complex medical histories including cardiac complications of OSA, neuromuscular disorders, obesity, failure to thrive, or craniofacial abnormalities,1 as these patients may be at higher risk of respiratory compromise.
Postoperative analgesia should also be approached with caution, as postoperative opioid administration has been associated with respiratory compromise in OSAS patients. A prospective study of 22 children showed that children with severe OSAS preoperatively (O2 saturation nadir <85%) required less morphine postoperatively than patients with milder disease, which suggests that recurrent hypoxemia may lead to increased narcotic sensitivity.33
Weight Gain Associated with Adenotonsillectomy for Obstructive Sleep Apnea
AT has been associated with weight gain after surgery. As described in the 1990s, weight gain was generally regarded as favorable for children undergoing treatment of OSAS that may have caused failure to thrive. However, later studies suggested that normal weight and even overweight patients showed accelerated weight postoperatively.34
A recent large prospective cohort study of 3963 children showed that AT performed before age 7 was associated with obesity at age 8 years (odds ratio of 2.89; confidence interval [CI] 1.74–4.79). Adenoidectomy alone was also associated with obesity, but the association was not as strong (odds ratio 2.19; CI 1.17–4.11).35 A systematic review of nine studies, including a total of almost 800 children, was performed to study AT as a risk factor for childhood obesity.36 BMI increased from 5.5 to 8.3%, standardized weight score increased in 46 to 100% of patients, and corrected weight increased in 50 to 75% of the patients after AT. Interestingly, morbidly obese patients (those defined as having weight of 130 to 260% of peers) showed no change postoperatively. While there are limitations to this study, it supports the theory that children gain more weight than normally expected postoperatively, suggesting a link between AT and weight gain.
Another study shows that preschool aged children who underwent AT increase the calories they are consuming daily in the postoperative period, and consume more foods that are high in sugar and fat. Although more data are required, this study suggests a link between AT and increased caloric intake, which could help to explain why children gain weight after the procedure.
Persistent Obstructive Sleep Apnea after Adenotonsillectomy
Although AT is the first line of treatment for pediatric SDB, a significant number of patients will have persistent symptoms. A systematic review by Friedman et al in 2009 showed that only 60 to 66% of children were cured of OSAS after adenotonsillectomy, with cure defined as an AHI <1 and <5.37 Most children were improved by PSG criteria, but this review focused on otherwise healthy children, where adenotonsillectomy is expected to have the most benefit. Obese children are at even higher risk for persistent OSAS. A meta-analysis showed a complete resolution of PSG parameters in only 10 to 25% of obese children after adenotonsillectomy, as compared with 70 to 80% of normal weight children.38
Children with more severe OSAS may be at increased risk for persistent disease following adenotonsillectomy. A study of 79 healthy children undergoing adenotonsillectomy showed that 36% of children with severe preoperative OSAS had persistent PSG abnormalities.39 Other factors that may place patients at high risk for persistence of disease include chromosomal disorders such as Down syndrome, craniofacial and neuromuscular anomalies, as well as African American race (Table 7.3).
Table 7.3 Conditions Associated with Increased Risk of Persistent OSA in Children
Black (African American) or other ethnicity
Craniofacial abnormalities—including Down syndrome
Hypotonia—including cerebral palsy
OSA, obstructive sleep apnea.
1. Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome. American Academy of Pediatrics. Clinical practice guideline: diagnosis and management of childhood obstructive sleep apnea syndrome. Pediatrics 2002;109(4):704–712
2. 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(6):827–832
3. Lumeng JC, Chervin RD. Epidemiology of pediatric obstructive sleep apnea. Proc Am Thorac Soc 2008;5(2):242–252
4. Nolan J, Brietzke SE. Systematic review of pediatric tonsil size and polysomnogram-measured obstructive sleep apnea severity. Otolaryngol Head Neck Surg 2011;144(6):844–850
5. Wilson K, Lakheeram I, Morielli A, Brouillette R, Brown K. Can assessment for obstructive sleep apnea help predict postadenotonsillectomy respiratory complications? Anesthesiology 2002;96(2):313–322
6. Yellon RF. Is polysomnography required prior to tonsillectomy and adenoidectomy for diagnosis of obstructive sleep apnea versus mild sleep disordered breathing in children? Laryngoscope 2010;120(5):868–869
7. 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
8. Olutoye OA, Watcha MF, Andropoulos DB. Pediatric obesity: observed impact in the ambulatory surgery setting. J Natl Med Assoc 2011;103(1):27–30
9. Shott SR, Amin R, Chini B, Heubi C, Hotze S, Akers R. Obstructive sleep apnea: Should all children with Down syndrome be tested? Arch Otolaryngol Head Neck Surg 2006;132(4):432–436
10. Rosen D. Some infants with Down syndrome spontaneously outgrow their obstructive sleep apnea. Clin Pediatr (Phila) 2010;49(11):1068–1071
11. Nashed A, Al-Saleh S, Gibbons J, et al. Sleep-related breathing in children with mucopolysaccharidosis. J Inherit Metab Dis 2009;32(4):544–550
12. Randhawa PS, Ahmed J, Nouraei SR, Wyatt ME. Impact of long-term nasopharyngeal airway on health-related quality of life of children with obstructive sleep apnea caused by syndromic craniosynostosis. J Craniofac Surg 2011;22(1):125–128
13. Hermann NV, Kreiborg S, Darvann TA, Jensen BL, Dahl E, Bolund S. Early craniofacial morphology and growth in children with unoperated isolated cleft palate. Cleft Palate Craniofac J 2002;39(6):604–622
14. Afsharpaiman S, Sillence DO, Sheikhvatan M, Ault JE, Waters K. Respiratory events and obstructive sleep apnea in children with achondroplasia: investigation and treatment outcomes. Sleep Breath 2011;15(4):755–761
15. Suresh S, Wales P, Dakin C, Harris MA, Cooper DG. Sleep-related breathing disorder in Duchenne muscular dystrophy: disease spectrum in the paediatric population. J Paediatr Child Health 2005;41(9-10):500–503
16. Cohen SR, Lefaivre JF, Burstein FD, et al. Surgical treatment of obstructive sleep apnea in neurologically compromised patients. Plast Reconstr Surg 1997;99(3):638–646
17. Villa MP, Malagola C, Pagani J, et al. Rapid maxillary expansion in children with obstructive sleep apnea syndrome: 12-month follow-up. Sleep Med 2007;8(2):128–134
18. Cozza P, Gatto R, Ballanti F, Prete L. Management of obstructive sleep apnoea in children with modified monobloc appliances. Eur J Paediatr Dent 2004;5(1):24–29
19. Kuhle S, Urschitz MS. Anti-inflammatory medications for obstructive sleep apnea in children. Cochrane Database Syst Rev 2011;(1):CD007074
20. Goldbart AD, Goldman JL, Veling MC, Gozal D. Leukotriene modifier therapy for mild sleep-disordered breathing in children. Am J Respir Crit Care Med 2005;172(3):364–370
21. Marcus CL, Rosen G, Ward SL, et al. Adherence to and effectiveness of positive airway pressure therapy in children with obstructive sleep apnea. Pediatrics 2006;117(3):e442–e451
22. Fauroux B, Lavis JF, Nicot F, et al. Facial side effects during noninvasive positive pressure ventilation in children. Intensive Care Med 2005;31(7):965–969
23. McGinley B, Halbower A, Schwartz AR, Smith PL, Patil SP, Schneider H. Effect of a high-flow open nasal cannula system on obstructive sleep apnea in children. Pediatrics 2009;124(1):179–188
24. Joshua B, Bahar G, Sulkes J, Shpitzer T, Raveh E. Adenoidectomy: long-term follow-up. Otolaryngol Head Neck Surg 2006;135(4):576–580
25. Brietzke SE, Kenna M, Katz ES, Mitchell E, Roberson D. Pediatric adenoidectomy: what is the effect of obstructive symptoms on the likelihood of future surgery? Int J Pediatr Otorhinolaryngol 2006;70(8):1467–1472
26. 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
27. 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
28. Eviatar E, Kessler A, Shlamkovitch N, Vaiman M, Zilber D, Gavriel H. Tonsillectomy vs. partial tonsillectomy for OSAS in children—10 years post-surgery follow-up. Int J Pediatr Otorhinolaryngol 2009;73(5):637–640
29. Powell NB, Zonato AI, Weaver EM, et al. Radiofrequency treatment of turbinate hypertrophy in subjects using continuous positive airway pressure: a randomized, double-blind, placebo-controlled clinical pilot trial. Laryngoscope 2001;111(10):1783–1790
30. Lin AC, Koltai PJ. Persistent pediatric obstructive sleep apnea and lingual tonsillectomy. Otolaryngol Head Neck Surg 2009;141(1):81–85
31. Prager JD, Hopkins BS, Propst EJ, Shott SR, Cotton RT. Oropharyngeal stenosis: a complication of multilevel, single-stage upper airway surgery in children. Arch Otolaryngol Head Neck Surg 2010;136(11):1111–1115
32. Schaaf WE Jr, Wootten CT, Donnelly LF, Ying J, Shott SR. Findings on MR sleep studies as biomarkers to predict outcome of genioglossus advancement in the treatment of obstructive sleep apnea in children and young adults. AJR Am J Roentgenol 2010;194(5):1204–1209
33. Brown KA, Laferrière A, Lakheeram I, Moss IR. Recurrent hypoxemia in children is associated with increased analgesic sensitivity to opiates. Anesthesiology 2006;105(4):665–669
34. Soultan Z, Wadowski S, Rao M, Kravath RE. Effect of treating obstructive sleep apnea by tonsillectomy and/or adenoidectomy on obesity in children. Arch Pediatr Adolesc Med 1999;153(1):33–37
35. Wijga AH, Scholtens S, Wieringa MH, et al. Adenotonsillectomy and the development of overweight. Pediatrics 2009;123(4):1095–1101
36. Jeyakumar A, Fettman N, Armbrecht ES, Mitchell R. A systematic review of adenotonsillectomy as a risk factor for childhood obesity. Otolaryngol Head Neck Surg 2011;144(2):154–158
37. Friedman M, Wilson MN, 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
38. Costa DJ, Mitchell RB. Adenotonsillectomy for obstructive sleep apnea in obese children: a meta-analysis. Otolaryngol Head Neck Surg 2009;140(4):455–460
39. Mitchell RB. Adenotonsillectomy for obstructive sleep apnea in children: outcome evaluated by pre- and postoperative polysomnography. Laryngoscope 2007;117(10):1844–1854