OVERVIEW: What every practitioner needs to know

Are you sure your patient has obstructive sleep apnea? What are the typical findings for this disease?

Obstructive sleep apnea should be suspected in children who snore, have restless sleep or show labored breathing and/or apnea. Other nocturnal symptoms include sweating, enuresis, parasomnia (sleep walking and talking) and night terrors.

Daytime symptoms include mouth-breathing and other symptoms of adenotonsillar hypertrophy, daytime sleepiness, behavior problems (irritability, oppositional behavior and, in school-aged children, poor academic performance, inattention and hyperactivity), morning headaches and poor somatic growth.

Typical signs and symptoms:

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Snoring- The hallmark of Obstructive Sleep Apnea Syndrome (OSAS) is repetitive complete or partial obstruction of the upper airways, leading to airflow cessation or limitation. The indicator of increased upper airway resistance is snoring at night. Snoring frequently occurs in children, with an average incidence of about 10%-12%. In epidemiological studies, snoring was reported in 96% of children with OSAS. With the exception of young infants, children with OSAS often snore loudly and continuously. Occasionally choking noises can be heard.

Difficulty breathing – Because initiation of breathing is normal in OSAS children, the diaphragm contracts, pushing the abdomen outwards and allowing the lungs to expand and fill with air. However, because of the upper airway obstruction, air cannot flow into the lungs and the chest is sucked in due to the negative intra-thoracic pressure. This causes paradoxical breathing that can be described by the parents as retractions, increased respiratory effort, difficulty breathing or “seesaw breathing”. Sometimes actual apnea is observed.

Restless sleep- reported in almost 80% of children with OSAS. Frequently, children will change positions overnight to assume the position that will relieve airway obstruction, such as hyper-extended neck or sitting upright propped upon pillows.

Other nocturnal symptoms: nocturnal sweating, enuresis, parasomnias (such as sleep walking and talking), nightmares and night terrors.

Daytime symptoms- usually stem from the underlying cause for the obstruction or from its complications:

(a) Adenotonsillar hypertrophy may lead to mouth-breathing, frequent upper respiratory infections, recurrent ear infections and hearing and speech impairment.

(b) Sleepiness, tiredness and fatigue – can be seen occasionally and usually in older children (estimated at 33% of children). However, it is not as prevalent as in adults with OSAS.

(c) In younger children, the daytime manifestation of fragmented, un-restful sleep will be inattention and disruptive behavior. In young children, it can manifest as persistent fussiness, inconsolability and oppositional behavior. In school-aged children, poor academic performance, inattention and hyperactivity, as well as mood disorders, can be seen.

(d) Morning headaches – usually strongest upon awakening and disappear by late morning. Unclear etiology.

(e) Growth – in young children, OSAS can present as poor growth. However, with the increase in incidence of obesity, more and more children with OSAS are overweight and obese. Correction of OSAS many times will accelerate growth and weight gain.

Physical Exam:

Beyond the routine physical exam, special attention should be given to evaluation of body habitus and the upper airways.

Height, weight and BMI are a very important part of evaluation for OSAS. As the Cleveland Family Study showed, elevated BMI is a strong risk factor for OSAS. The risk of OSAS increases by 12% for each 1 kg/m2 increase in body mass index.

General observation: Mouth-breathing and adenoidal faces, hyponasal voice is a clue of nasal obstruction and a muffled voice is suggestive of adenotonsillar enlargement. Retrognathia, micrognathia, or midfacial hypoplasia can be seen by examination of the lateral profile.

Nose: should be assessed for septal deviation, mucosal thickening, polyps, and patency of vestibule.

Oral cavity: evaluate the relationship between the tongue, uvula, tonsils and palate. Large tongue, high-arched or elongated palate, or a low dependent palate may predispose to OSA. The Mallampati classification (See Figure 1) is useful in this assessment, particularly in older and obese children. The tonsillar size is important in the physical assessment, as it plays a significant causative role in younger children with OSA. Tonsils are usually described according to their appearance on simple oral exam: minimally visible, visible to the pillars, visible beyond the pillars, and visible to the uvula (kissing tonsils).

Figure 1.
The Mallampati Classification.

Neck circumference: was found to correlate with prevalence of OSA, as well as with the severity of OSA. In adolescents, neck circumference of more than 15″ in females and 16″ in males should trigger an evaluation of OSAS.

Cardiac exam: is usually normal; however, in advanced and severe cases, evidence of pulmonary hypertension manifested by a loud second pulmonary heart sound has been reported. In addition, routine monitoring of systemic hypertension should be done.

Risk Factors for OSAS:

(1) Family history – there is a 3-4 fold excess risk of OSAS in members of families with a proband with OSAS.

(2) Ethnicity – African Americans have increased propensity to OSAS. They are approximately three and a half times more likely to have sleep-disordered breathing (SDB) than the general population. Studies have also shown increased OSAS in Mexican Americans, Pacific Islanders and East Asians.

(3) BMI – Obese children are 4-5 times more likely to have OSAS than non-obese children.

(4) Disorders of craniofacial abnormalities – such as Pierre Robin sequence and Down syndrome.

(5) Prematurity – premature infants are predisposed to upper airway obstruction and oxygen desaturations during sleep due to poor airway stability and highly compliant chest wall.

(6) Certain genetic syndromes – Treacher Collins, Crouzon syndrome.

(7) Neurologic disorders – spinal muscular atrophy and Duchenne muscular dystrophy.

(8) Lower airway disease – recent studies show a positive relationship between upper and lower airway disease, as is seen by an increased incidence of OSAS in children with asthma, chronic cough and history of sinus problems.

What other disease/condition shares some of these symptoms?

The term ‘‘sleep-disordered breathing’’ (SDB) in children refers to a group of respiratory disorders that occur or are exacerbated during sleep. These include the following: central apnea, apnea of prematurity, hypoventilation, and the spectrum of obstructive hypoventilation disorders.

Apnea of prematurity – central in nature. Particularly prevalent at early gestational age (24-32 weeks) and usually resolve by full term. It is thought to be related to immaturity of the respiratory centers. Periodic breathing is another form of apnea of a brief duration, followed by rapid breathing for 10-15 seconds before the next brief apnea. Periodic breathing decreases in frequency with age, but can be seen up to 12-18 months of age. It is known to respond well to oxygen supplementation or distension of the airway with positive pressure.

Apnea of infancy – periodic breathing and central apnea during sleep are less likely in normal term infants. Possible causes are: gastroesophageal reflux, pharyngeal incoordination, seizures, infection, heart disease, congenital central hypoventilation syndrome, metabolic disorders and brain tumors. Several reports describe the association between OSAS and apparent life-threatening event (ALTE) during early infancy.

Central hypoventilation – defined as an increase in PaCO2 due to decrease in central nervous system ventilatory drive. Central hypoventilation can be primary, as seen in congenital central hypoventilation syndrome (CCHS), or secondary to neurological disorders such as Arnold-Chiari malformation, anoxic brain injury, brain stem tumors and encephalitis. Other causes can be metabolic diseases, hypothyroidism and drugs.

Peripheral hypoventilation – due to restrictive lung disease. Can be due to diseases that involve the lung, such as pulmonary fibrosis, and lung restriction due to chest wall deformities or respiratory muscle weakness. In both conditions, significant hypoventilation and oxyhemoglobin desaturations can be seen, especially during Rapid Eye Movement (REM) sleep.

Primary snoring – defined as snoring with no associated apneas or hypopneas. In the recent official pediatric sleep statement, this condition is considered to be benign. However, new evidence is emerging showing OSAS complications in this group of patients. More studies need to be done to determine if primary snoring should be considered a disorder.

What caused this disease to develop at this time?

Genetics of OSAS- patients with OSAS often have a family history of the condition. There is clear evidence that a positive family history of OSAS is an important risk factor for an elevated apnea-hypopnea index (AHI) and associated symptoms such as snoring and daytime sleepiness. Overall heritability for OSAS is 0.30 to 0.40. Candidate genes of OSAS inheritance can be related to areas encoding: obesity and body fat distribution, craniofacial morphology, ventilatory control patterns and control of sleep and circadian rhythms.

Epidemiology of OSAS – pediatric OSAS is a different entity than the adult disease. Of the many children with habitual snoring (10%-12% in the general population), approximately 2%-3% will have clinically relevant disease. Therefore, the ratio between symptomatic habitual snoring and obstructive sleep apnea (OSA) is 3-5:1.

OSAS is seen most frequently between the ages of 2-6 years of age, when the tonsils and adenoids are at their maximal size. However, with the accelerated increase over the last two decades in the prevalence of pediatric obesity, there was substantial change in the cross-sectional demographic and anthropometric characteristics of the children being referred for evaluation of habitual snoring.

Childhood obesity used to account for 15% of pediatric OSA; it is currently the reported cause of 50% of OSAS cases. Dr. David Gozal offered to divide the children with OSAS into 2 groups: type I and type II OSAS. Type I is associated with marked tonsillar and/or adenoid hypertrophy and failure to thrive. These are younger children, show equal male: female incidence, and have more hyperactive and attention disorders as a consequence. Type II is associated primarily with obesity and milder upper airway lymphoid hyperplasia. These children are older and show male predominance. Daytime symptoms are different and include excessive daytime sleepiness, depression and social withdrawal. They also more likely to have metabolic syndrome and cardiovascular complications, such as left ventricular hypertrophy and systemic hypertension.

“Secondary OSAS” refer to the group of patients with OSAS secondary to an underlying medical condition, such as craniofacial abnormities and or neurological disorders affecting upper airway shape, configuration, and collapsibility during sleep.

What laboratory studies should you request to help confirm the diagnosis? How should you interpret the results?

Evaluation of OSAS:

(1) Screening test – Simple and convenient, screening questionnaires for children with OSAS based on clinical history have been studied for their ability to identify OSAS, but have not been able to precisely distinguish between OSAS and primary snoring. Validated questionnaires are available; the most frequently used questionnaire is by Chervin et al. and is called the Pediatric Sleep Questionnaire (PSQ). It includes 22 questions about children’s sleep and is mostly used as a tool in research settings.

(2) Home audio and video recording – can efficiently screen for OSAS, but still have low specificity.

(3) Continuous pulse oximetry monitoring – The finding of intermittent oxygen desaturations during sleep in children is highly suggestive of OSAS. However, considering difficulties with the technical application of this method at home and understanding that many children may have multiple arousals due to obstructive events without the hypoxemia, this technique has significant limitations.

(4) Home monitoring – Unattended home studies in children with OSAS have been improving in quality. However, the utility of unattended home studies in children to assess OSAS in a non-research setting and across all age groups has not yet been established.

(5) Laboratory testing – polycythemia and compensatory acidosis might be present, even though usually corrected once the child is awake. In obese children signs of metabolic syndrome can be seen with dyslipidemia and insulin resistance. OSAS is associated with a group of proinflammatory and prothrombotic factors that have been identified as important in the development of vasculopathy. Such studies in children note endothelial dysfunction, and increase in C-reactive protein, IL-6, fibrinogen, and plasminogen activator inhibitor. It is possible that biological markers, such as urinary or serum protein patterns, will identify children at risk for developing cardiovascular or neurocognitive morbidity in the presence of OSAS.

(6) Polysomnography (PSG) – Polysomnography (See Figure 2) has been recommended by an expert consensus panel assigned by the American Academy of Pediatrics (AAP) as the gold-standard test for establishing the presence and severity of SDB in children. The polysomnographic variables monitored and recorded during PSG (See
Table I) include but are not limited to the following:

Figure 2.
Pediatric hooked up for a polysomnography

1. EEG activity: current American Academy of Medicine (AASM) recommendations are F4-M1, C4-M1 and O2-M1 with backup (F3-M2, C4-M1, O2-M1).

2. Eye movements (electrooculogram) from electrodes placed near the outer canthus of each eye.

3. Submental electromyographic (EMG) activity from electrodes placed over the mentalis, submentalis muscle, and/or masseter regions.

4. Rhythm electrocardiogram (ECG) with one lead II electrode.

5. Respiratory effort, by chest-wall and abdominal movement via strain gauges, piezoelectric belts, inductive plethysmography, impedance or inductance pneumography, endoesophageal pressure.

6. Nasal and/or oral airflow via thermistor, nasal pressure transducer, or pneumotachograph or inductance plethysmography.

7. Oxygen saturation (SpO2) via pulse oximetry including wave form, with an averaging time of no more than 3 seconds.

8. End tidal CO2 or transcutaneous CO2 monitors.

9. Body position by sensor or by direct observation.

10. Limb movement (right or left leg) via EMG.

11. Snoring recording or vibration (frequency and/or volume).

12. Audio/video recording by infrared or low-light equipment.


In polysomnography, measurements of breathing during sleep are done through measurement of flow via the nose, respiratory effort via the chest and abdominal belts, oxyhemoglobin saturations, gas exchange through end tidal CO2 monitor and appearance of the child during the night and especially during apnea episodes, as seen via the video. The polysomnogram (See
Figure 3) is reviewed for the following events (See
Figure 4):

Figure 3.
Typical 30 seconds epoc of a polysomnogram

Figure 4.
In this slide there are three respiratory patterns that are shown:
The upper panel shows obstructive apnea as seen by cessation of flow with continuous chest and abdominal movement.
The middle panel demonstrates central apnea, as seen by cessation of flow associated with lack of chest and abdominal movements.
Lower panel demonstrates periodic breathing, as seen by the alternating central apnea and hyperventilation patterns.

Obstructive apnea – An obstructive apnea is scored when there is a >90% decrease in the airflow amplitude and the event lasts for at least 2 breaths, with continued respiratory effort throughout the whole event.

Obstructive hypopnea – scored when there is a >50% drop in airflow signal amplitude compared with the previous baseline amplitude. The event must last at least two missed breaths and should be associated with an arousal, awakening, or a >3% oxygen desaturation.

Central apnea – the cessation of flow is associated with absent inspiratory effort throughout the duration of the event, and one of the following is present: (1) the event lasts 20 seconds or more, or (2) the event is associated with an arousal, an awakening, or a >3% desaturation.

Hypoventilation – is determined if more than 25% of the total sleep time is spent with end tidal CO2 measurements above 50 torr.

Apnea index (AI) – the number of obstructive and central apneas per hour of sleep.

Apnea hypopnea index (AHI) – the number of central and obstructive apnea and hypopneas per hour of sleep.

Obstructive apnea index – the number of obstructive apnea events per hour of sleep.

Central apnea index – the number of central events per hour of sleep.

Upper airway resistance syndrome (UARS) – A respiratory disorder of sleep associated with snoring but no apnea, causing excessive daytime sleepiness due to arousals and sleep fragmentation.

Normal oxygenation – Published normative data in children show that basal oxygen saturation values range from 95%-100%, oxygen saturation nadir can normally be as low as 84%-86% saturation, and the number of desaturations of 4% or more per hour can range from 0 to 2.6 per hour. Mild desaturation (90%-93%) is relatively common in children during sleep.

Would imaging studies be helpful? If so, which ones?

Usually radiological studies are not necessary to diagnose OSAS. However, the following studies may be helpful in certain patients:

(1) Lateral neck x-ray – done to assist with determining the size of tonsils and adenoids.

(2) Chest x-ray – in patients with significant OSAS or when cardiovascular complications are suspected, a chest x- ray may assist in determining cardiac size. Of course, the x-ray should be coupled with an EKG and followed by an echocardiography if any of these tests are positive.

Confirming the diagnosis

As suggested by the American Academy of Pediatrics in their clinical practice guidelines published in 2002, all children should be screened for snoring during a health supervision visit. The screening should include direct questions obtained by history, such as the presence of snoring with labored breathing, observed apnea, restless sleep, neurobehavioral abnormalities or sleepiness, and evaluation for alterations in growth or physical findings that may support the diagnosis of OSAS. If any of the above is present, further consideration should be made regarding additional risk factors for OSAS, beyond adenotonsillar hypertrophy and obesity. These include craniofacial or syndromic conditions affecting upper airway anatomy or neurologic conditions affecting upper airway motor control.

Children without identifiable additional risk factors should be referred for polysomnography, whereas children with risk factors should be referred to a sleep specialist for further evaluation before polysomnography. The diagnosis of OSAS should be made by the guidelines outlined in the previous section. As mentioned, particular attention is paid to the following measures: apnea and hypopnea indices, gas exchange abnormalities, and the number of arousals related to respiratory events. Once the diagnosis of OSAS is made, a clinical treatment plan can be outlined on the basis of polysomnography results, history, and physical findings. Clinical sequelae for children with OSAS may be dependent on the type and severity of polysomnographic abnormalities.

If you are able to confirm that the patient has obstructive sleep apnea, what treatment should be initiated?

OSAS treatment:

(1) Adenotonsillectomy (T&A) – is considered the first line of therapy in pediatric OSAS. It is indicated in all OSAS patients with evidence of adenoidal or tonsillar hypertrophy. It was thought that T&A brought a cure to 75%-100% of normal non-obese patients. However, a recent multi-center retrospective study had shown that from a group with mixed OSAS severity, only about 30% of patients had complete resolution of OSAS. It was concluded that T&A leads to significant improvements in indices of sleep-disordered breathing in children. However, residual disease is present in a large proportion of children after T&A, particularly among older (>7 yr) or obese children.

The postoperative complications of T&A in patients with severe OSAS are significant and, according to AAP guidelines, these patients should be observed overnight in a medical facility after their surgery.

(2) When T&A fails or is not indicated, the next recommended intervention is non-invasive positive pressure, or continuous positive airway pressure (CPAP). CPAP is administered with an electronic device that delivers constant air pressure via a nasal or facial mask, leading to mechanical stenting of the airway and improved functional residual capacity in the lungs. The pressure requirement varies among individuals; thus, CPAP must be titrated in the sleep laboratory before prescribing the device, and periodically readjusted thereafter. CPAP is a long-term therapy and requires frequent clinician assessment of adherence and efficacy. Attention to compliance with this therapy is crucial.

(3) Other surgical options – because of the poor adherence rates to CPAP, other surgical procedures are now offered to patients with OSAS. Possible surgical procedures are: Uvelopharyngopalatoplasty (UPPP) and mandibular or maxillary advancement surgery. These surgeries are mostly used in children with craniofacial anomalies.

(4) Dental appliances – can be used in pediatric patients with OSAS. The treatment should be done by a pediatric dentist who has knowledge and experience in sleep medicine. Oral appliances are popular and more tolerated then CPAP, however, they are mostly recommended for mild to moderate OSAS when CPAP failed.

(5) Tracheostomy – bypasses the obstruction and relieves OSAS. However, tracheostomy care over a long period of time is complex and demanding and therefore reserved as a last resort.

(6) Intranasal corticosteroids – limited evidence suggests that intranasal corticosteroids may significantly improve nasal obstruction symptoms in children with moderate to severe adenoidal hypertrophy. This improvement may be associated with a reduction in adenoid size. The long-term effect of intranasal corticosteroids in these patients remains to be defined.

(7) Leukotriene inhibitors (LT-I) – because of the strong correlation of OSAS with inflammatory markers as well as the findings of high levels of leukotrienes in tonsils taken from children with OSA, the efficacy of LT-I was tested in one study. The study looked at the response of adenoidal hypertrophy and OSA to treatment with LT-I. The study showed improvement in the apnea-hypopnea index in patients with mild OSA. A more robust effect of LT-I was shown in in vitro treatment of adenoidal tissue with local LT-I.

What are the adverse effects associated with each treatment option?


What are the possible outcomes of obstructive sleep apnea?

Complications of longstanding OSAS are diverse and involve different body systems:

(1) Metabolic sequelae:

  • (a) Weight – Failure to thrive in younger patients with type I OSAS. Obesity is seen in older, type II patients. Interestingly, weight gain is seen in both groups after correction of OSAS.
  • (b) Decreased insulin-like growth factor
  • (c) Altered growth hormone secretion
  • (d) Insulin resistance
  • (e) Elevated C-reactive protein
  • (f) Hyperchlolesterolemia
  • (g) Elevated transaminases

(2) Cardiovascular sequelae:

  • (a) Autonomic dysfunction
  • (b) Abnormal heart rate variability
  • (c) Systemic hypertension
  • (d) Left ventricular dysfunction
  • (e) Pulmonary hypertension
  • (f) Elevated vascular endothelial growth factor

3) Neurocognitive sequelae leads to impairment in:

  • (a) Cognition
  • (b) Hyperactivity
  • (c) Excessive daytime sleepiness
  • (d) Memory loss
  • (e) Loss of executive function
  • (f) Impaired attention
  • (g) Poor school performance
  • (h) Aggressive behavior
  • (i) Depression
  • (j) Moodiness
  • (k) Decreased quality of life

Even mild OSAS or even primary snoring is associated with adverse neurodevelopment outcomes.

(4) Increased utilization of medical services

It is important to emphasize to families that children with OSAS, in most cases, do not die in their sleep. The body’s compensatory mechanisms get into action once there is a notion of airway obstruction (as sensed by the large negative intra-thoracic pressures), which leads to arousal and regaining of airway muscle strength with opening of the airway. The significant morbidity seen in OSAS is from the above-mentioned complications, as well as morbidity and mortality associated with daytime sleepiness, such as falling asleep while driving.

What causes this disease and how frequent is it?


In a widely distributed questionnaires to parents asking about snoring was found that:

1. 1.5% to 6% of parents reported their child was ‘‘always’’ snoring

2. 0.2% to 4% of parents reported observed apneic events during sleep

3. 4% to 11% reported sleep-disordered breathing by varying constellations of symptoms on the questionnaire

However, OSA diagnosed by varying criteria on diagnostic studies was 2% to 4%. Overall prevalence of parent-reported snoring by any definition in meta-analysis oscillate between 8%-12% in different studies.

There are 3 main groups of patients at risk for having OSAS:

(1) Children with tonsillar and/or adenoidal hypertrophy – these tend to be younger, usually 2-6 years of age, an age that correlates with maximal adenotonsillar hypertrophy. The children are usually low-weight, and their daytime symptoms are mostly hyperactivity and inattention. This is still the most common reason for pediatric OSA.

(2) A growing population of children with OSAS are the children with obesity. They tend to be older, have higher BMI and develop a picture of metabolic syndrome that includes insulin resistance, hyperlipidemia and abnormal liver function. Their daytime symptoms are more of excessive daytime sleepiness. In addition to impaired neurocognitive function and externalizing disorders, they also suffer from mood disorders and low self esteem.

(3) Children with congenital anomalies, syndromes and neuromuscular weakness that predisposes them to airway obstruction during sleep.


There is no real seasonality to OSA. However, because of its relationship to enlargement of lymphoid tissue, parents might see and report it more in the winter and spring months.

Inflammation and OSAS:

A new notion in the understanding of OSAS is the fact that the disease is not purely caused by mechanical obstruction of the airway (by tonsils and adenoids in type I or fat pads or low lung volumes in type II OSAS), but OSAS is a systemic disease with a significant inflammatory component, as is reflected in the following reports:

The inflammatory nature of OSAS was initially demonstrated when tonsils were compared between children who had T&A for OSA, as opposed to tonsils taken out for recurrent tonsilitis. In OSA-tonsils, there is inflammatory cell proliferation and increased expression of pro-inflammatory cytokines and other inflammatory mediators (e.g., TNF-a, IL-6, and IL-1a) that is not seen in the other group. Further, studies examining exhaled breath condensate and induced sputum in children with OSAS show the up-regulation of localized inflammatory processes in upper airway tissues. In addition, elevated levels of C-reactive protein are present in children with OSAS, and these levels decrease after effective management of the OSA.

Therefore, two mechanisms have been proposed to explain the morbid consequences of OSA: (a) oxidative stress and (b) activation of inflammatory processes. Both, however, are further modulated by genetic, lifestyle and environmental factors.

How do these pathogens/genes/exposures cause the disease?

In OSAS, there are two main processes that result from the nature of the disease. These are:

1. Intermittent hypoxemia and re-oxygenation coupled with hypercarbia

2. Sleep fragmentation

Both process cause increase oxidative stress, activate inflammatory pathways, and increase sympathetic nervous activity, leading to the above-mentioned OSAS complications: metabolic disease, cardiovascular disease and neurocognitive impairment. This end organ damage is mediated by increased proinflammatory cytokines, increased adipokines, such as leptin, and changes in metabolic functions, such as elevated levels of circulating insulin, glucose, cholesterol and LDL.

Other clinical manifestations that might help with diagnosis and management

Primary snoring:

An interesting new development in the research of pediatric OSA is the notion that habitual snoring is not benign. As mentioned before, the term “primary snoring” is defined as habitual snoring that is not associated with apnea, hypopneas or gas exchange abnormalities on an overnight PSG.

A study by O’Brien el al. drew attention to the neurocognitive derangements in children with primary snoring. In 2009, another study showed the cardiovascular complications associated with children with primary snoring. In that study, Li Am et al. showed elevated diastolic blood pressure during the night in children who had PSGs, showing primary snoring.

The neurocognitive and cardiovascular complications were milder compared with the ones seen in OSA patients, but they support the idea that these two conditions are a continuum and raise the question – is all snoring abnormal and should we refer to snoring as a symptom of disease, such as wheezing or stridor? The American Thoracic Society (ATS) recommendations still state that primary snoring is a condition that does not indicate specific intervention.

What complications might you expect from the disease or treatment of the disease?

Treatment success for T&A:

As mentioned before, in older reviews from a decade ago looking at T&A results for OSAS, success rates of surgery were thought to be excellent and T&A was thought to be the cure for cases of pediatric OSA. However, a recent multicenter study looking at success rates of T&A in the cure of OSA showed results that are less encouraging.

In children with mild OSA (<5 AHI), T&A was curative in about 65%-70% of both obese and non-obese children. In children with moderate OSA (5>AHI<10), full cure was seen in only 55%-60% of cases in both obese and non-obese groups. And in severe OSA cases (AHI >10), complete cure was only achieved in 35%-45% of both obese and non-obese children. Therefore, the study’s authors concluded that the “study suggests that T&A is associated with significant improvements in sleep-disordered breathing in most children. However, older children, obese children, and non-obese children with either severe OSAS or with asthma are at an increased risk for residual OSAS. Under such circumstances, pre- and post- T&A sleep studies should be conducted, at least among the high-risk groups identified.”

Are additional laboratory studies available; even some that are not widely available?

Magnetic resonance imaging (MRI) is a non-invasive and radiation-free method to evaluate upper airway morphology. There are studies both in adults and pediatric OSA patients looking at the anatomical factors that predispose to OSA. Anatomical characteristics have a large influence on the severity of OSA. Extra large soft tissue morphologies in children, bony structure malformations during growth, reduced pharyngeal airway lumen in adults, and excessive fat deposition in the upper airway soft tissues directly influence the severity of OSA in patients. Currently this tool is used in a research setting, but has potential advantages in evaluation and tailoring appropriate treatment for individual patients with OSAS.

How can obstructive sleep apnea be prevented?


What is the evidence?

Recommended literature:

“Clinical practice guidelines: diagnosis and management of childhood obstructive sleep apnea syndrome. Section on Pediatric Pulmonology, Subcommittee on Obstructive Sleep Apnea Syndrome”. Pediatrics. vol. 109. 2002. pp. 704-12. (This is the latest set of practice guidelines provided by the AAP for the diagnosis and management of OSAS.)

Katz, ES, D’Ambrosio, CM. “Pediatric obstructive sleep apnea syndrome”. Clin Chest Med. vol. 31. 2010. pp. 221-34. (This is a recent review paper that discusses nicely the diagnosis, epidemiology, pathophysiology, complications and management of OSA. This would be a good review for the general practitioner to read.)

Capdevila, OS, Kheirandish-Gozal, L, Dayyat, E, Gozal, D. “Pediatric obstructive sleep apnea: complications, management, and long-term outcomes”. Proc Am Thorac Soc. vol. 5. 2008. pp. 274-82. (Another review paper that discusses the newer developments in pediatric OSAS, with specific emphasis on the metabolic derangements and inflammatory aspects, as well as the change in the nature of the disease with the increasing rate of obesity among pediatric patients.)

Bhattacharjee, R, Kim, J, Kheirandish-Gozal, L, Gozal, D. “Obesity and obstructive sleep apnea syndrome in children: a tale of inflammatory cascades”. Pediatr Pulmonol. vol. 46. 2011. pp. 313-23.

Gozal, D. “Sleep, sleep disorders and inflammation in children”. Sleep Med. vol. 10. 2009. pp. S12-S16. (The above two review papers discuss OSAS as an inflammatory disease, both from Dr. David Gozal’s group.)

Muzumdar, H, Arens, R. “Diagnostic issues in pediatric obstructive sleep apnea”. Proc Am Thorac Soc. vol. 5. 2008. pp. 263-73. (To learn more about polysomnography and other diagnostic issues in OSAS, this review is very comprehensive and updated.)

Bhattacharjee, R, Kheirandish-Gozal, L, Spruyt, K. “Adenotonsillectomy outcomes in treatment of obstructive sleep apnea in children: a multicenter retrospective study”. Am J Respir Crit Care Med. vol. 182. 2010. pp. 676-83. (This is the article discussing the success rate of T&A.)

Redline, S, Tishler, PV, Schluchter, M. “Risk factors for sleep-disordered breathing in children: associations with obesity, race, and respiratory problems”. Am J Respir Crit Care Med. vol. 159. 1999. pp. 1527-32. (This is the reference for the Cleveland Family Study looking at risk factors for pediatric OSAS.)

Ongoing controversies regarding etiology, diagnosis, treatment