Important OSA definitions
Obstructive apnea
Cessation of ventilation (i.e., no airflow), despite respiratory effort, for 10 s or two breath cycles in older children or 6 s or 1.5–2 breaths in younger children
Obstructive hypopnea
Decrease in airflow by 50%, despite respiratory effort, during the same time or breath cycles, associated with a desaturation or arousal
AHI
The total number of apneic events plus hypopneas per hour of sleep
RDI
Another term for the AHI
AI
Describes the number of arousals per hour of sleep
Abbreviations: AHI, apnea/hypopnea index; AI, arousal index; OSA, obstructive sleep apnea; RDI, respiratory disturbance index.
OSA in children is part of a continuum of sleep-disordered breathing (SDB). The clinically mildest form of SDB is primary snoring. The child has episodes of stertorous breathing during sleep but no ventilation abnormalities. As the severity progresses, upper airway resistance syndrome (UARS) develops. In the UARS, there is increased respiratory effort during breathing with ventilation abnormalities but without apnea or hypopnea. OSA is the most severe form of SDB. The sleep disturbance has a profound negative impact on the child’s growth and development. The correlation between severity of OSA and its consequences on the child are unpredictable. A mild OSA may have a profound impact, whereas a severe OSA may not. Other factors such as preexisting medical conditions, duration of the OSA, and the child’s age seem to be important.
19.2 Epidemiology and Prevalence
Constant snoring is noticed by parents in approximately 10% of healthy children. It is usually self-limiting within 2 years in 50% of these children. OSA is observed in 2 to 3% of children. 2 Though some children with OSA may improve in time, the negative neurocognitive and developmental impact may be such that intervention is warranted, and observing the child with overt OSA for possible improvement with natural history is inappropriate. This highlights the importance in differentiating simple snoring from OSA.
Pediatric OSA occurs mostly in infants and children below 6 years of age with a peak incidence at 3 to 4 years of age. This coincides with the physiological peak in adenotonsillar hypertrophy. There is another peak incidence in infants less than 1 year old due mostly to predisposing conditions such as craniofacial abnormalities, but early adenotonsillar hypertrophy causing OSA in infants has been described and should be considered. 3
Pediatric OSA is a different pathophysiological entity from its adult counterpart. OSA has a very great impact on the child and family because developmental issues are of great importance ( ▶ Table 19.2).
Adults | Children |
Obese | Failure to thrive |
Not a mouth breather | Mouth breather |
Male > female | Male = female |
Daytime somnolence | Attention deficit hyperactivity disorder |
Non REM | REM |
No adenotonsillar hypertrophy | Adenotonsillar hypertrophy |
Surgery usually not curative, requires CPAP | Surgery usually curative |
Abbreviations: CPAP, continuous positive airway pressure; OSA, obstructive sleep apnea; REM, rapid eye movement. | |
19.3 Physiology of Normal Sleep
Normal sleep has five stages: stages 1 to 4 are increasing levels of sleep with increased slowing of brain activity as seen on electroencephalography (EEG) and a progressive decrease in muscular tone. Stage 5 is rapid eye movement (REM) sleep when the brain shows increased activity and dreaming takes place. Paradoxically, in REM sleep, there is a further decrease in muscular tone, possibly a failsafe mechanism to prevent running away from our dreams. Other sleep-induced physiological changes are increased upper airway resistance, decreased minute ventilation, and decreased ventilatory responses to hypoxia and hypercapnia. Thus, in the predisposed child during sleep, obstructive episodes lead to a marked impact on breathing and gas exchange. Because muscle tone decreases progressively from stage 1 through 4 sleep, reaching a nadir during REM sleep, children are particularly vulnerable to airway obstruction during REM sleep. This vulnerability is especially prominent in children because a proportionally larger part of their sleep is in REM.
19.4 Pathophysiology of Obstructive Sleep Apnea
The upper airway is a collapsible tube. The collapsibility of the tube depends on diameter and compliance. The variables influencing diameter relate to skeletal and soft-tissue abnormalities. Compliance is influenced by muscle tone and central nervous system (CNS) drive. Upper airway obstruction in children with OSA is multifactorial. The three main predisposing factors are as follows:
Hypertrophy of tonsils and adenoids or other tissue in the airway.
Craniofacial anomalies.
Oropharyngeal neuromuscular abnormalities.
Any one factor or a combination of these factors can cause OSA.
William Osler wrote in “The Principles and Practice of Medicine,” 1892: “Chronic enlargement of the tonsillar tissue is an affection of great importance, and may influence in extraordinary ways the mental and bodily development of children … At night, the child’s sleep is greatly disturbed, the respirations are loud and snorting and there are sometimes prolonged pauses …” “The child responds slowly to questions…impossible to fix attention for long at a time … looks sullen … The influence upon mental development is striking.”
OSA is to be differentiated from central apnea where the cause is related to a CNS lesion, and cessation of breathing is not due to obstruction. The pathophysiology of central apnea is related to lack of respiratory drive usually due to insensitivity to elevation of the partial pressure of carbon dioxide (CO2) at the level of the brainstem. Central and obstructive apnea may coexist especially in neurologically impaired children. This is termed mixed obstructive/central apnea.
19.5 Effects of Obstructive Sleep Apnea
19.5.1 Metabolic
The intermittent ventilatory disturbance in OSA results in hypercarbia and hypoxia with an impact on the child’s metabolism. This may result in endothelial dysfunction. Many metabolic disturbances have been found including elevation in C-reactive protein, insulin resistance, hypercholesterolemia, elevated serum transaminase, decreased insulin-like growth factor (IGF), and decrease in growth hormone (GH) secretion. These metabolic sequelae present clinically as failure to thrive (FTT) in children but are also observed in obese children with OSA. 4
19.5.2 Increased Health Care Utilization
A common misconception is that the tonsils and adenoids are important in protecting a child from illness and cause no adverse effects.
Tonsillectomy and adenoidectomy (T+A) not only improves OSA but also results in a drastic reduction in health care utilization after surgery.
This was seen across all health care utilization measures including a reduction of visits to the emergency room (ER) and pediatrician, medications, and days of work missed by parents. 5
19.5.3 Neurobehavioral Deficits
A hallmark of adult OSA is daytime somnolence. In children, the neurobehavioral sequelae are different. Most remarkable is attention deficit hyperactivity disorder most probably as a result of fragmented sleep in OSA. Other findings noted are reduced scholastic achievements and reduction in overall cognitive ability (intelligence quotient). Surgical intervention (T+A) has been shown to improve some of these deficits. 6 In a recent randomized study of adenotonsillectomy versus watchful waiting for OSA in school-aged children (Childhood Adenotonsillectomy Trial), surgery did not significantly improve attention or executive function as measured by neuropsychological testing but did reduce symptoms and improve secondary outcomes of behavior, and quality of life. 7
19.5.4 Cardiovascular Dysfunction
Although now rarely seen, severe OSA over a prolonged period will result in pulmonary hypertension and cor pulmonale.
Early intervention has reduced these clinical findings. However, in a child with long-standing severe OSA, an echocardiogram should be considered with referral to a pediatric cardiologist for further assessment as needed. If pulmonary hypertension is found, there is an increased surgical and anesthetic risk, and postoperative management on a high dependency unit (HDU) or even a pediatric intensive care unit (PICU) may be required. OSA in children may also result in blood pressure dysregulation as a result of increased sympathetic tone. 4 There is recent evidence that pediatric OSA predisposes to long-term adult cardiovascular morbidity, which is presumably caused by chronic low-grade inflammation and endothelial dysfunction. However, it is a cofactor with obesity. 8
19.5.5 Growth Retardation
FTT in children with OSA is now less commonly observed due to earlier diagnosis. The causes are GH–IGF axis dysregulation, poor food intake, and increased energy expenditure during sleep. In children with FTT, weight gain is observed following T+A probably as a result of decreased energy expenditure during sleep. 4
19.5.6 Decreased Quality of Life
Studies using validated questionnaires reflecting quality of life in children with OSA have shown a decreased quality of life. Health-related quality of life as assessed by the OSA-18 questionnaire showed decreases in the domains of the following:
Sleep disturbance.
Physical symptoms.
Emotional symptoms.
Daytime functioning.
Caregiver concerns.
These were greatly improved following surgery (T+A). 9
19.6 Clinical Presentation
19.6.1 The History
OSA has a negative impact on the child’s health, but the child who is seen in clinic may appear healthy and happy. It’s during sleep that the drama occurs. Careful history is of the utmost importance.
Since most children with OSA are snorers, a key question to the child’s parent or caregiver is: “Does your child snore?” This simple question is a good screening test for pediatric OSA.
Further questions regarding sleep should focus on restless sleep, effortful breathing, and cessation of breathing, all of which are helpful in defining the severity of OSA. Daytime symptoms such as behavioral problems, FTT, and chronic mouth breathing may also be elicited.
Most children with OSA are habitual snorers, whereas not all that snore have OSA.
Enquiry about snoring is an excellent question during history taking and can be used as a screening tool for OSA with high sensitivity but low specificity. Other questions related to sleep are as follows:
Are there chest efforts while breathing?
Are there episodes of cessation of breathing and gasping?
Is the sleep restless?
Further questions are related to the sequelae of OSA: weight, growth curve, FTT, and behavioral and developmental issues especially attention deficit. Bed-wetting may also be a result of OSA. ▶ Table 19.3 summarizes daytime and nighttime symptoms of pediatric OSA.
Nighttime symptoms | Daytime symptoms |
Noisy breath (snoring) | Hypersomnolence |
Mouth breathing | Fatigue |
Difficulty breathing | Hyperactivity |
Paradoxical breathing | Delayed development |
Breathing pauses | Learning problems |
Sweating | “Adenoid facies” |
Restless sleep | Pectus excavatum |
Frequent movements | Failure to thrive |
Unusual postures | |
Frequent awakening | |
Bed-wetting | |
Abbreviation: OSA, obstructive sleep apnea. | |
19.6.2 Physical Examination
A full ENT examination must be performed when examining the child with a history of OSA. It’s not only about tonsils and adenoids.
Examine the nasal airway for masses, anatomical deviations, and the occasional foreign body.
Palpate the neck for masses.
Look for maxillofacial features such as dysplasia, micro- or retrognathia, macroglossia, etc.
Examine for fluid in the middle ear; this can be due to nasopharyngeal obstruction.
Examine the oral cavity.
The examination of the oral cavity is important but may be difficult in children who have a basic aversion to tongue depressors and will usually put up a fight. This can be avoided by establishing a rapport with the child and even offering a bribe. But at times, the only way to achieve a good examination is to have the parent firmly but gently hold the child while gently opening the mouth and inserting the tongue depressor. Good lighting with a headlight will also help. The oral cavity can then be examined.
Tonsil size can be graded from 0+ to 4+:
0+: post-tonsillectomy.
1+: tonsils inside the pillars.
2+: tonsils outside the pillars.
3+: tonsils reach the midpalate.
4+: tonsils reach the uvula, also termed kissing tonsils ( ▶ Fig. 19.1).
Look at the palate for signs of a submucous cleft palate such as bifid uvula, maxillary notch, and zona pellucida (a clear strip of mucosa in the midline of the palate caused by the muscular diastasis of the tensor veli palatini). Children with submucous cleft palate are at particular risk of velopharyngeal insufficiency (VPI) after surgery.
Flexible nasopharyngolaryngoscopy is an integral part of the ENT examination in children. A small diameter pediatric scope is needed to reduce discomfort. In older children, cooperation can usually be attained by engaging the child in the examination. Younger children will require a strong hug by the parent. Spraying the nasal cavity with a combination of local anesthetic (lidocaine 1%) and decongestant (pseudoephedrine) can be helpful. With a combative child full of nasal discharge, the examination will lack value and may have to be deferred. In a child with OSA and small tonsils, the endoscopic examination is extremely important in order to elucidate the cause of obstruction.
Fig. 19.1 Grade 4+ obstructing tonsils (kissing tonsils).
19.7 Investigation and Diagnosis
Is history alone enough in the diagnosis of OSA? Obviously, in an otherwise healthy child with incessant snoring, observed cessation of breathing and extreme effort of breathing while asleep, especially when coinciding with FTT, is sufficient for diagnosis and prompt treatment. Most children are not in such an extreme category of OSA, making diagnosis more difficult. In multiple studies, history and physical examination were inadequate in diagnosing OSA when compared to full overnight sleep studies, polysomnography (PSG). 10 This cumulated data questions the physician’s ability to make therapeutic decisions based on history alone.
19.7.1 Sleep Studies
The gold standard for diagnosis of OSA is considered to be a complete overnight PSG (or “full sleep study”). When asleep, recordings of the child’s EEG, pulse rate, oxygen saturation, blood pressure, respiratory rate, apneic and hypopneic episodes, limb movements, and simultaneous video recording are obtained. The referring physician receives the data and summary, the bottom line being the respiratory disturbance index (RDI) or apnea/hypopnea index (AHI), representing the number of apneas and hypopneas per hour of sleep. 11
There is no consensus on normative data, but in most centers, an RDI of 0 to 1.5 per hour is considered normal, RDI of 1.5 to 5 per hour is mild OSA and RDI of 5 to 10 per hour is moderate. Severe OSA with more than 10 episodes per hour requires prompt attention and intervention.
Many parents when asked say their child’s sleep in the laboratory was not the same as at home. The environment is not always comfortable for the child and parent. The examination also entails a cost and, in many centers, a waiting list. This raises a question of necessity especially since the delay in attaining a sleep study may have an adverse effect on the child’s health because of the delay in treatment. In many cases, the clinical diagnosis is sufficient and PSG has no added value.
PSG should be reserved for when the diagnosis is unclear or for more complex cases.
Although there are no clear guidelines, suggested indications for PSG are summarized in Box 19.1. This has led to increasing interest in looking at simpler reliable investigative techniques.
Box 19.1 Indications for PSG
Neurologic disease.
Age < 2 years.
Increased surgical risk.
Borderline cases.
Craniofacial anomalies.
Continued symptoms after surgery.
A UK multidisciplinary group looking at indications for adenotonsillar surgery for children with OSA suggested that “respiratory investigations” were appropriate in the following circumstances 12:
Diagnosis of OSA uncertain.
Age less than 2 years.
Weight less than 15 kg.
Down’s syndrome.
Cerebral palsy.
Hypotonia or neuromuscular disorder.
Obesity (body mass index more than 2.5 or SDS more than 99th percentile for age and gender).
Comorbidity, for example, congenital heart disease, lung disease, and mucopolysaccharidosis.
Failure to respond to T+A surgery.
“Ambulatory” or “Home” Sleep Study
This is an appealing solution with the child sleeping in his/her natural environment and requiring fewer resources. The study is technically challenging since children tend to remove the leads and there is no technician to monitor and correct the deficient data, so an ambulatory PSG in children has no real advantage.
Overnight Pulse Oximetry
Pulse oximetry in sleep measures oxygen saturation but fails to show obstructive events that result in fragmentation of sleep and respiratory effort that do not result in decreased oxygen saturation. These events may have a profound negative effect on the child but are missed.
Pulse oximetry alone is inadequate for diagnosis of OSA in children.
Some suggest that oximetry can be used as screening for SDB and as a crude measure of severity. The McGill oximetry scoring system is a useful way to grade severity of OSA, as predicted from overnight pulse oximetry, on a 1 to 4 scale 13:
Score 1 (normal OSA/inconclusive): up to three drops in oxygen saturation between 85 and 90%.
Score 2 (mild OSA): three or more drops in oxygen saturation below 90%, up to three of which are between 80 and 85%.
Score 3 (moderate OSA): three or more drops in oxygen saturation below 85%, up to three of which are below 80%.
Score 4 (moderate OSA): three or more drops in oxygen saturation below 80%.
The failure to be able to identify hypopneas and respiratory efforts that do not cause desaturations but can cause morbidity limits the usefulness of pulse oximetry.
Video Home Recording of Sleep
Known as “the poor man’s sleep study” this is a reasonable compromise. It allows for the child to sleep in her home environment and for the physician to observe snoring, periods of apnea and respiratory effort. This is a qualitative and not a quantitative examination such as is seen in the sleep laboratory, and there are some limitations. It is impractical for the physician to observe the whole night, and the chosen segment may not be representative. The quality of the home recording is often suboptimal. To improve results, the parents should be guided on technical details of the recording, which should commence approximately 2 hours after sleep. A small night light should be on in the room so that the child’s chest and face can be seen clearly. The video recorder should be placed on a tripod or stationary stand, not handheld. Usually, 30 minutes of recording is sufficient. 14
With the widespread use of smartphones, we see more parents who present video clips of their child sleeping. Though helpful at times, we must remember the limitations.
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