6 Pediatric Obstructive Sleep Apnea
Abstract
As in adults, pediatric obstructive sleep apnea (OSA) is characterized by partial or complete obstruction of the upper airway during sleep. However, definitions, prevalence, pathophysiology, and diagnostic procedures differ substantially from adult standards. Pediatric OSA is associated with multiple adverse neurodevelopmental and cardiometabolic consequences. It is common in healthy children and occurs with a higher incidence among obese children, and among kids with syndromic, neurologic, or craniofacial diseases.
Medical interventions include weight loss, nasal corticosteroids, and other allergic treatments. Oral devices and continuous positive airway pressure are also used to treat pediatric OSA. Standard surgical treatment is adenotonsillectomy (T&A). Most healthy children respond favorably to adenotonsillectomy as first-line treatment. Tonsillotomy seems to provide comparable results as tonsillectomy with decreased postoperative pain, readmissions to hospital, and complications. Persistent OSA after T&A has frequently been described in obese kids or children with underlying craniofacial deformities or syndromic or other severe comorbidities. In these children, other kinds of surgeries might be helpful.
6.1 Diagnosis
6.1.1 Introduction
Obstructive sleep-disordered breathing (SDB) is a syndrome of upper airway dysfunction during sleep, characterized by snoring and/or increased respiratory effort secondary to increased upper airway resistance and pharyngeal collapsibility. It includes a spectrum of clinical entities such as primary snoring, upper airway resistance syndrome, obstructive hypoventilation, and obstructive sleep apnea (OSA) syndrome (▶Table 6.1). 1
The term obstructive sleep-disordered breathing in children is used when symptoms of intermittent upper airway obstruction during sleep are present, but the severity of airway obstruction has not been defined by objective measurements such as polysomnography (PSG). 2
Obstructive sleep apnea syndrome (OSAS) is characterized by repetitive episodes of upper airway obstruction that occur during sleep, usually associated with reduction in blood oxygen saturation. 3 It affects both children and adults.
In contrast, simple snoring is not associated with repetitive episodes of upper airway obstructions, (or with <5 events/hour) arousals from sleep, and low oxygen saturation in arterial blood. The most common definitions of habitual snoring are: “snoring present often/frequently” for more than three or four nights per week. 4
6.1.2 Prevalence
Primary snoring and OSA are common conditions in the pediatric population. The estimated prevalence of primary snoring in children ranges from 8 to 27%. 5 Lumeng and Chervin published a meta-analysis of studies with a prevalence of habitual snoring of 7.45% (95% CI 5.75–9.61). 4 OSAS is less common. The estimated prevalence of OSAS in children is ranging from 1 to 5%. 6
6.1.3 Clinical Finding
The clinical symptoms of pediatric obstructive SDB during the sleep are snoring, sweating, breathing by mouth, apneas, and enforced breathing. The head is extended and the neck flexed during the sleep. The snoring is often with intermittent pauses, snorts, or gasps.
Daytime sleepiness is mostly not the leading symptom in young children. Failure to thrive, hypertension, cardiac dysfunction, and systemic inflammation are associated to OSA (▶Table 6.2). 5
History | |
Frequent snoring (≥3 nights/wk) | |
Labored breathing during sleep | |
Gasps/snorting noises/observed episodes of apnea | |
Sleep enuresis (especially secondary enuresis) | |
Sleeping in a seated position or with the neck hyperextended | |
Cyanosis | |
Headache on awaking | |
Daytime sleepiness | |
Attention deficit/hyperactivity disorder | |
Learning problem | |
Physical examination | |
Underweight or overweight | |
Tonsillar hypertrophy | |
Adenoidal facies | |
Micrognathia/retrognathia | |
High-arched palate | |
Failure to thrive | |
Hypertension | |
Data from Marcus et al. 5 | |
6.1.4 Physical Examination
Hypertrophy of the Tonsils and of the Adenoid Tissue
Hypertrophy of the tonsils and of the adenoid tissue seems to be the most common cause of primary snoring and OSA in children. The hypertrophy of the tonsils and adenoids causes narrowing of the airway during sleep when the muscles of the pharynx relax. This leads to partial or complete obstruction of the airway. 7 MRI studies have shown that the size of the adenoids and tonsils in children with OSA is significantly increased compared with healthy controls. 8 Children with OSA have been found to have significantly more collapsible upper airways during sleep than children without OSA. 9
Allergic Rhinitis and Nasal Hypertrophy
Allergic rhinitis may be associated with SDB. Nasal turbinate hypertrophy increases the risk of mild OSA. 10
Craniofacial Morphological Characteristics
In a meta-analysis, Flores-Mir et al identified that craniofacial characteristics such as steep mandibular plane, vertical direction of craniofacial growth, and retrusive chin are related to OSA. 11 However, another meta-analysis from the same year suggested that the differences between children with SDB and controls are of marginal clinical significance. 12
Midface Deficiency Syndrome and Mandibular Hypoplasia
Midface deficiency syndromes such as Apert syndrome, Crouzon syndrome, Pfeiffer syndrome, and unrepaired or repaired cleft palate, and marked mandibular hypoplasia (Pierre Robin sequence, Treacher Collins syndrome, Nager syndrome, Stickler syndrome, and juvenile idiopathic arthritis) are associated with increased risk of obstructive SDB. 1
Neuromuscular disorders and uncontrolled epilepsy are related to a high risk for OSAS and nocturnal hypoventilation. 13
Complex abnormalities (achondroplasia, Chiari malformation, Down’s syndrome, Ehlers-Danlos syndrome, mucopolysaccharidoses, and Prader-Willi syndrome) have been related to OSAS and alveolar hypoventilation. 1
Down’s Syndrome
Children with Down’s syndrome are predisposed to OSAS and hypoventilation because of midfacial and mandibular hypoplasia, shortened palate, relative macroglossia, narrow lumen of the nasopharynx, and pharyngeal hypotonia. Parents may not report SDB symptoms. Main risk factors for OSAS in children with Down’s syndrome include age less than 8 years, male gender, and tonsillar hypertrophy. 14
Obesity
Obesity in children is a well-established risk factor for SDB. Childhood obesity is defined as a body mass index (BMI) more than 95th percentile for age and gender. 6 Obesity is an increasing health problem in children. Since 1980, the prevalence of overweight and obesity has increased remarkably in developed countries; 23.8% of boys and 22.6% of girls were overweight or obese in 2013, compared with 16.9% of boys and 16.2% of girls in 1980. 15
The NANO study, a cross-sectional, prospective multicenter study, assessed the contribution of obesity and adenotonsillar hypertrophy in pediatric OSA and found that 46.6% of obese children in their community had an apnea–hypopnea index (AHI) of more than 1 per hour per total sleep time. 16 The prevalence of pediatric OSAS in obese children varies in other studies from 19 to 61%. 17 In postpubertal adolescents an association between OSA and the metabolic syndrome has been shown. 18
Blood Pressure
A greater mean blood pressure (BP) variability during wakefulness and sleep, a higher night/day BP ratio, and a reduced nocturnal dipping were observed in children with OSA as compared with normal controls. 19
But a meta-analysis by Zintzaras and Kaditis did not demonstrate an association between OSAS and BP. 20
Systemic Inflammation
There is emerging evidence that OSA is a disease with chronic low-grade systemic inflammation and increased oxidative stress which likely leads to end-organ morbidities. 13 Nasal nitric oxide (nNO), a marker of airway inflammation, is elevated in children with primary snoring and OSAS as compared with a healthy control group. The nNO level is not correlated with disease severity. It is probably due to the local mechanism. 21 The peripheral Th17/Treg balance is skewed toward Th17 predominance, further suggesting a systematic proinflammatory milieu in OSA. The Th17/Treg ratio correlates with severity of OSA. Adenotonsillectomy (ATE) reverses this Th17/Treg imbalance and reduces serum inflammatory cytokine levels. 22 Plasminogen activator-inhibitor 1 levels and monocyte chemoattractant protein 1 levels have been found to be significantly raised in obese children with OSA compared with obese children without OSA. 16
Loffredo et al suggests that even children with primary snoring have significantly higher serum isoprostanes and soluble NOX2-dp levels and display evidence of endothelial dysfunction compared with healthy controls. 23
Prematurity and Family History of Obstructive Sleep Apnea
A history of prematurity is associated with an increased risk of OSA, and there is some evidence that a family history of OSA may also be a risk factor. 1
Behavioral and Neurocognitive Morbidities
Children with OSAS have been linked with behavioral and neurocognitive morbidities. 24 Published data from the Tucson Children’s Assessment of Sleep Apnea Study (TuCASA study) showed that even mild OSA and primary snoring are associated with hyperactivity, difficulties concentrating, attention problems, and impulsivity. 25 Results of the TuCASA study revealed a significant association of SDB with behavioral problems (aggression, lower social competency, poorer communication, and/or diminished adaptive skills).
Nocturnal Enuresis
There appears to be a significant prevalence of OSAS in children with enuresis. Nocturnal enuresis is defined as urination during sleep in children older than or equal to 5 years, which is when nocturnal bladder continence is developmentally expected. Enuresis can occur in any stage of sleep and at any time of the night. 26 , 27 Brooks and Topol found that children referred to for suspected SDB who had a respiratory disturbance index (RDI) of more than 1 had a higher prevalence of enuresis (47%) as compared with those who had an RDI of less than or equal to 1 (17%). 28
The reason for the enuresis may be due to the inhibitory effects of OSA on arousal response to changes in bladder pressure, or effects of elevated brain natriuretic peptide (BNP) levels which affect the renin-angiotensin pathway, vasopressin, and excretion of sodium and water. 29
Children with enuresis, particularly those who are obese or resistant to standard treatments, should be assessed for symptoms and physical findings suggestive of SDB, and if any symptom is present, a PSG is recommended. 27
Quality of Life
Children with OSAS had poorer scores in the Child Health Questionnaire than healthy children. Children with OSAS had similar scores to those of patients with juvenile rheumatoid arthritis. 30
6.1.5 Diagnostic Workup
Patient Anamnesis
The clinical practice guideline of the American Academy of Pediatrics recommends that pediatricians should ask for snoring at each health maintenance medical visit. 5 This question is a sensitive, albeit nonspecific screening measure that is quick to perform. Additional questions about the symptoms, which are listed in ▶Table 6.2, should be added to narrow this large group of snoring children. The clinical evaluation does not establish the diagnosis. Clinical signs and symptoms are unable to accurately predict pediatric OSAS. Taking patient’s history has a predictive value of 65% as compared to PSG. 31
The parent-filled questionnaire assesses symptoms of OSA, such as snoring, excessive daytime sleepiness, attention problems, and hyperactive behavior in children between ages 2 and 18 years. Its sensitivity and specificity for diagnosing OSA in otherwise healthy children are 78 and 72%, respectively. Questionnaires may be useful in predicting OSA-related neurobehavioral morbidity and its improvements after ATE. 32
Physical examination may be normal when the child is awake, and the size of the tonsils cannot be used to predict the presence of OSAS. The predictive value is not higher than 46% with the clinical examination alone. 31
Other clinical parameters such as demographics, physical examination, findings, and parent-reported questionnaires also do not discriminate between different levels of OSAS based on PSG parameters. 33
Further recommendations from the American Academy of Pediatrics are as follows: If a child or adolescent snores on a regular basis and has any of the complaints or findings shown in▶Table 6.2, clinicians should either (1) obtain a PSG (Evidence Quality A, Key action strength: Recommendation), or (2) refer the patient to a sleep specialist or otolaryngologist for a more extensive evaluation (Evidence quality D, Key Action strength: Option). 5
Technical Measurements
Even today, the gold standard test for OSAS is the overnight, fully attended, in-laboratory PSG in a sleep facility. Despite this fact, there is a shortage of sleep laboratories with pediatric expertise. PSG is not available worldwide. Even in the high-industrial countries PSG is not available in all regions. Laboratory PSG studies of children are expensive, and parents and their young children, particularly school-aged children, are often hesitant to spend a night in the unfamiliar setting of a sleep laboratory. In an effort to simplify the diagnostic process and to make this process more accessible and convenient, a number of unattended multichannel devices have been assessed in pediatric patients (▶Table 6.3). 34
According to the American Academy of Sleep Medicine (AASM) guidelines, unattended devices are defined as multichannel type 2 or type 3 devices. Type 2 monitoring devices can be used to perform full PSG outside a laboratory. 35 The major difference between type 2 and 3 devices and type 1 devices is that the former two types do not require a technician. Type 3 monitoring devices (respiratory polygraphy [RP]) do not record the signals needed to determine sleep stages. Their channels include two respiratory variables (e.g., respiratory movement and airflow), a cardiac variable (e.g., heart rate or an electrocardiogram), and an arterial oxygen saturation. There is the possibility that the AHI may be underestimated due to missed hypopneas resulting in arousals, but not desaturation. Type 4 monitoring devices are also known as continuous single or dual bioparameter devices. They record one or two variables (typically arterial oxygen saturation and airflow). They can also be used without a technician. Oximetry studies have a high specificity but low sensitivity in the diagnosis of pediatric OSA. The rate of false-negative or inconclusive results is high. 36
In a meta-analysis about unattended type 2 and type 3 devices, Certal et al described a satisfactory overall diagnostic accuracy of unattended multichannel devices as compared with the gold standard (full PSG type 1 devices). These type 2 and 3 devices are claimed as useful and valid tools for OSA screening in children. 37 The type 2 and 3 devices may theoretically be ubiquitously accessible and more cost-effective. The results may be more representative of the child’s typical night’s sleep at home. Ambulatory monitoring with unattended devices is considered reliable for the diagnosis of OSA in particular groups of patients.
Nevertheless, unattended type 2 and 3 diagnostic tests have been shown to have weaker positive and negative predictive values than PSG. If an alternative test fails to demonstrate OSAS in patients with high pretest probability, full PSG should be sought. 37
The overnight, fully attended, in-laboratory PSG measurements include electroencephalography (EEG), pulse oximetry, oronasal airflow, abdominal and chest wall movements, partial pressure of carbon dioxide, and video recording (▶Table 6.4). A comprehensive list of respiratory indications for PSG in children according to the AASM is presented in ▶Table 6.5. The indications are divided into three groups: standard, guideline, and option. A standard level of recommendation has high degree of clinical certainty with use of level 1 evidence or overwhelming level 2 evidence, whereas a guideline has a moderate degree of clinical certainty. An option has uncertain clinical use. 38 The American Academy of Otolaryngology/Head and Neck Surgery (AAO/HNS) has a more selective policy for obtaining PSG (▶Table 6.6). For action statement number 1, the rationale is to avoid unnecessary interventions in children with higher surgical risk and facilitate postoperative planning. For action statement number 2, the intent is to minimize the risk of either over- or undertreatment. The AAO/HNS recommendations for postoperative monitoring were addressed in action statement number 4, but were based only on observational studies. 39
PSG in children should be performed and interpreted in accordance with the recommendations of the AASM Manual for the Scoring of Sleep and Associated Events. 40
According to the latest version of the International Classification of Sleep Disorders (ICSD-3), PSG criteria for diagnosis are either (1) one or more obstructive events (obstructive or mixed apnea or obstructive hypopnea) per hour of sleep or (2) obstructive hypoventilation, as manifest by partial pressure of carbon dioxide (PaCO2) more than 50 mm HG for 25% of sleep time, together with snoring, paradoxical thoracoabdominal movement, or flatting of the nasal airway pressure waveform implying flow limitation. 3 In international studies the definition of the AHI varied a lot and the AHI threshold is contested.
The cut off for AHI defining OSA ranged from 1 to 5 episodes per hour. Most studies used a criterion of more than or equal to 2 but less than or equal to 5 episodes per hour. 17 At the moment there is lack of consistency in the definition of pediatric OSA and in terminology used in the literature. Most sleep centers consider an obstructive AHI less than or equal to 1 per hour total sleeping time (TST) to be normal, AHI more than 1 but less than or equal to 5 to be mild OSA, AHI more than 5 but less than or equal to 10 to be moderate OSA, and AHI more than 10 per hour TST as severe OSA (▶Table 6.7).
There is an agreement in the international literature that an AHI more than 5 per hour requires treatment.
Drug-Induced Sleep Endoscopy
The first pediatric drug-induced sleep endoscopy (DISE) was published in 1990. 42 In the literature there is a wide variability regarding the indications and the way how it should be performed. Recently Friedman published a multi-institutional study over the current state of pediatric DISE. 43 The majority of respondents required that a PSG needs to be carried out prior to DISE. The predominant indication for DISE is residual OSA after ATE. Recent evidence has demonstrated that up to 30% of children undergoing ATE for treatment of OSA will have significant residual disease, likely due to obstruction at locations besides the tonsils or adenoids. 44 A variety of anesthetic protocols and agents are used for DISE. None of the agents adequately simulate rapid eye movement (REM) sleep. 45 During the DISE the airway sites from the nasal cavity to the glottis were regularly examined, whereas the bronchi were not. 43 Adjunctive maneuvers were frequently being performed, including a chin lift to simulate closed-mouth breathing and a jaw thrust to simulate a mandibular-repositioning device. 46 Different scoring system for DISE had been published, but a consistent scoring system is not typically used. 44 , 47 DISE can either be performed as an isolated procedure or in combination with sleep surgery. In the latter case, the kind of sleep surgery is selected according to DISE findings. A staged approach allows for a detailed discussion of the planned sleep surgical procedure, which improves opportunities for shared exception recovery and results. 43 Alternatively, some families prefer to have interventions performed at the time of the DISE; in these situations, the surgeon must discuss the risks and benefits of each potential sleep procedure, whereas the family must accept the uncertainty of what procedures will be performed on the day of the procedure. 43
Key Points
Prevalence of snoring in children is estimated to be 8 to 27%, prevalence of pediatric OSA 1 to 5%.
Pediatric OSA is associated with various health impairments.
Obesity and adenotonsillar hypertrophy are associated with pediatric OSA. However, physical examination alone is not sufficient to diagnose pediatric OSA.
Several parent-reported questionnaires are helpful to screen for pediatric OSA.
Sleep studies are necessary to diagnose OSA free of doubt. Unfortunately pediatric PSG is both complex and hardly available. This is why unattended multichannel sleep studies can be used instead.
In uncomplicated cases a characteristic anamnesis in combination with an adenotonsillar hypertrophy confirmed through a physical examination of a child is sufficient to indicate an ATE as primary treatment for pediatric OSA. A sleep study is not required.
Other cases, and recurrent or persistent disease after ATE, require a sleep study prior to (revision) surgery.
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