INTRODUCTION

Obstructive sleep apnea (OSA), which essentially is difficulty breathing and sleeping at the same time, is a very common problem in the pediatric population. Despite being so common, OSA is a frequently missed diagnosis. It is not clear why OSA is not considered sooner in the differential diagnosis for a child who is experiencing snoring, irritability, hyperactivity, restless sleep, and chronic respiratory problems. Perhaps it is due to the relative infancy of the diagnosis of OSA. As recently as the early 1980s, OSA in children was considered a rare diagnosis. However, no matter what the reason, making an accurate and timely diagnosis is imperative because if left untreated, OSA can be associated with cognitive, behavioral, cardiovascular, and metabolic consequences. We are likely to realize in the near future and as outlined so exquisitely by Gozal et al. (Gozal & Kheirandish-Gozal, 2010) that the morbidity associated with OSA in the form of neurocognitive, cardiovascular and metabolic manifestations are interrelated. They are likely shaped by individual susceptibility, environment and lifestyle, and severity of OSA (Gozal & Kheirandish-Gozal, 2010). That places the responsibility on us as caregivers to identify problems early and to treat them accordingly.

It is therefore important that nurses and nurse practitioners receive adequate training and information regarding OSA. The knowledge gained from this training and information can help nurses and nurse practitioners identify symptoms of OSA in children. Identification of symptoms can ultimately lead to proper diagnosis and hopefully avoidance of complications associated with OSA.

EPIDEMIOLOGY

The diagnosis of OSA has steadily increased over the past decade, in large part due to increased awareness and screening, but also due to the number of centers that perform the diagnostic testing necessary to identify OSA. Current medical literature states OSA occurs in children of all ages, from toddlers to adolescents, with estimates of prevalence from 2 to 4% (Meltzer et al., 2010). The peak incidence of OSA is between the ages of 2 and 6 years, coinciding with the peak age of lymphoid hyperplasia, when the tonsils and adenoids reach their maximum size in relationship to the upper airway dimensions.

Habitual snoring occurs in up to 12% of the general pediatric population and in most children with OSA. However, a history of snoring is insufficient to diagnose OSA because not all children who snore have OSA (Perez & Davidson, 2008). OSA is equally common in boys and girls. However, following the onset of puberty, OSA is more common in males.

The incidence of pediatric OSA appears to be on the upswing. This is most likely due to the notable increase in child and adolescent obesity over the past decade. Recent studies have found that the risk of OSA among adolescents (age ≥ 12 years) increases 3.5-fold with each standard deviation increase in body mass. The risk of OSA was not significantly increased with increasing body mass in younger children (Kohler, 2009).

Among otherwise healthy children, adenotonsillar hypertrophy, obesity, and upper respiratory problems are conditions that predispose children to OSA (Lumeng & Chervin, 2008). Adenotonsillar hypertrophy is usually the result of multiple etiologies, the most common of which are proliferation of lymphoid tissue, recurrent upper respiratory infections, allergic irritants, chronic nasal obstruction, and pharyngeal edema from gastroesophageal reflux. These etiologies all have in common the feature of an anatomically or functionally narrowed upper airway. Other risk factors include respiratory problems such as sinusitis, chronic rhinitis, asthma, African American ethnicity, family history of OSA, and low socioeconomic status (Benninger & Walner, 2007).

Medical, neurological, or dental conditions that reduce airway size, affect the muscle control of the upper airway, or impact the collapsibility of the upper airway also place a child at an increased risk of OSA. Examples include the following:

• Cerebral palsy
  
• Down syndrome
  
• Craniofacial abnormalities (micrognathia, retrognathia, midface hypoplasia, Pierre–Robin syndrome)
  
• History of prematurity/low birth weight
  
• Muscular dystrophy
  
• Achondroplasia
  
• Orthodontic problems (high, narrow hard palate, malocclusions).

PATHOPHYSIOLOGY

OSA in children is a syndrome characterized by recurrent periods of elevated upper airway resistance with partial or complete intermittent airflow obstruction of the upper airway during sleep, and can be associated with snoring, episodic oxyhemoglobin desaturation, hypercapnia, and repeated arousals (Sheldon, Ferber, & Kryger, 2005). In order to understand the pathophysiology associated with disturbed nighttime sleep, one needs some understanding of normal nighttime sleep in children. There are expected norms for length of sleep time and sleep architecture based on age and development. An excellent review of such norms appears in Dr. Jodi Mindell’s Clinical Guide to Pediatric Sleep (Mindell & Owens, 2003).

It is presumed that sleep serves a restorative purpose, especially during deep non-REM stage N3 sleep. REM sleep is frequently spoken of in lay circles as “the deepest sleep,” but in fact the brain is as metabolically active during REM sleep as it is during wakefulness. Experts believe that REM serves a purpose of rehearsal and learning. For example, if in school we learn that 2 + 2 = 4, it is during REM sleep that such information is rehearsed and put into our internal “hard drive.” Accordingly, any disruption in the continuity, quality, or quantity of sleep can have major impacts on neurocognitive development (Gozal et al. 2007), learning and general well-being.

The most common cause for childhood OSA is adenotonsillar hypertrophy, but enlarged tonsils and adenoids alone do not account for the entire pathophysiological process. OSA is linked to a relationship between structural and neuromuscular variables within the upper airway. Though several studies show that children with OSA have enlarged tonsils and adenoids when compared to their age-matched cohorts, not every child with large tonsils has OSA, and some children have persistent OSA despite having a tonsillectomy and adenoidectomy. Thus, structural factors alone cannot be fully accountable for OSA (Au & Li, 2009). It is believed that OSA occurs in children because the size of their airway is small in relation to the size of their tonsils and adenoids. Furthermore, other issues such as neuromuscular tone, nasal airway anatomy, and mandibular and midface structure can all add to the effect that airway caliber has on OSA.

Airflow obstruction during sleep can be associated with hypoxemia and hypercarbia and the sequelae associated with these blood gas alterations. Much focus in recent years has been on the oxidative stress associated with intermittent hypoxemia as well as the vast hemodynamic changes that occur repetitively all night long secondary to arousals from sleep. The current thinking is that this pathophysiology sets the patient up for conditions of chronic inflammation such as asthma, metabolic dysfunction, and cardiovascular stress (Gozal & Kheirandish-Gozal, 2008).

Numerous studies have been published over the past 5 years describing the findings of increased levels of mediators of inflammation (Gozal et al., 2008; Gozal, 2009; Tauman, O’Brien, & Gozal, 2007). It is still not clear whether the inciting event for the inflammatory cascade is the arousal from sleep itself, independent of oxygenation, or whether the intermittent hypoxia is the trigger. No doubt this debate will continue for many years. Suffice to say, however, that there is a link connecting OSA, obesity, asthma, and cardiovascular disease (Gozal & Kheirandish, 2006; Gozal & Kheirandish-Gozal, 2008).

When it comes to arousals from sleep versus hypoxemia, it is unclear which of the two is more problematic. It is well described that children with OSA manifest poor school performance and other neurocognitive deficits (Kheirandish & Gozal, 2006). The question is whether the source of the problem is due to arousals from sleep or the effects of intermittent or persistent hypoxemia. It is likely a combination of both (Gozal & Kheirandish, 2006).

For years, it has been scrutinized as to whether snoring is an innocent sound or whether snoring in and of itself is problematic (O’Brien et al., 2004a). Studies have demonstrated that snoring, which is often described as “harmless” primary snoring (PS), is associated with elevated systemic blood pressures (Amin et al., 2004). In addition, PS is known to be associated with children scoring higher on scales of inattentiveness and impulsivity.

The presence of snoring may actually serve as a source of arousal from sleep, which the technology at hand may not yet to be able to pick up. The vibrations in the upper airway (which we call snoring) have been hypothesized to damage the neuromuscular end plate in the upper airway. This damage may then render the patient with diminished tone in the upper airway, which is one of the proposed mechanisms for OSA. At the very least, snoring indicates that there is an increase in upper airway resistance (Marshall, 2007) that begs further investigation. Thus, no degree of snoring should be considered normal.

SIGNS AND SYMPTOMS

OSA can masquerade as hyperactivity, poor school performance, exercise intolerance, asthma, and chronic cough. Therefore, snoring is not the only symptom associated with OSA. The following list outlines additional important symptoms that could be elicited during a sleep interview:

• Restless sleep
  
• Sweating
  
• Audible noisy breathing
  
• Mouth breathing
  
• Unusual sleeping positions
  
• Nightly awakenings
  
• Enuresis
  
• Early morning awakenings
  
• Difficulty waking up in the morning
  
• Late for school because of sleepiness in the morning
  
• Daytime sleepiness
  
• Poor focus in class
  
• Poor behavior in school or at home
  
• Hyperactivity
  
• Poorly responsive to attention deficit/hyperactivity disorder (ADHD) medications
  
• Poor school grades
  
• Daytime irritability
  
• Daytime napping (after the age of 5)
  
• Trouble falling asleep at night

It is clear to see that such a symptom list is extensive. However, any one of the above symptoms could be a clue toward identifying OSA. A number of the above symptoms deserve special attention. Restlessness, for example, may need to be elicited in a number of ways, especially if the child no longer spends any sleep time with the parent. For an older child, you can ask whether the sheets are all kicked off the bed by morning. For younger children who still spend some time (or a lot of time) sleeping with parents, you may hear parents make comments like

• I will never sleep with him again. He kicks me all night long.
  
• He circles the bed like a clock.
  
• We shared a bed in a hotel on vacation last week and he kept me up all night long.

In regard to sweating, parents can often be very dramatic about the amount of perspiration. They may describe children soaking the sheets with sweat, needing to change the sheets, or needing to change the pajamas. Sometimes, the history of sweating is masked by adaptations that the child has made over the years, such as sleeping without sheets or blankets, only sleeping in underwear, or sleeping with fans or air conditioners even during the wintertime.

Some unusual sleep positions that may need to specifically be asked about include sleeping with the neck hyperextended. In addition, sometimes toddlers and young children will sleep with knees under the chest and bottom up in the air. Raising or heaving of the shoulders and chest may also be described.

Enuresis is an important symptom. It is one of the most common problems seen in a pediatric primary care office and ranks near the top in terms of most troubling problems for a patient and family. While the exact mechanisms have not been identified, there is a strong link between nocturnal enuresis and OSA. Some proposed mechanisms include patients with OSA having increased levels of morning brain natriuretic peptide (Capdevila et al. 2008). Arousals, hypoxemia, and excessive sleepiness have also been suggested as potential causes. Regardless of the exact mechanism, for many patients, treatment for OSA has resulted in improvement or even complete elimination of nocturnal enuresis (Basha et al., 2005).

The following is a list of medical conditions that might be elicited by history and should raise concern about possible OSA:

• Poorly controlled asthma despite maximal medical therapy and appropriate environmental controls
  
• Obesity
  
• Insulin resistance
  
• Recurrent tonsillitis
  
• Gastroesophageal reflux
  
• Attention deficit disorder with or without hyperactivity
  
• Failure to sleep train despite appropriate efforts
  
• Unexplained nocturnal hypoxemia discovered during a hospitalization for asthma or other illness
  
• Persistent nocturnal enuresis despite all efforts at assessment and management
  
• Growth disturbance (unexplained by any other cause)
  
• Neurodevelopmental delays (unexplained by any other cause)

In addition to a detailed history, the physical exam can be very informative. Tonsils can be easily visualized and are often described as big or small. Tonsils can be scored on a scale of 1+ to 4+. Tonsils that are scored as 1+ and 2+ are frequently described as normal; 3+- and 4+-sized tonsils are described as enlarged. However, the following points should be kept in mind:

In addition to obtaining lateral head X-rays or performing direct visualization with nasal endoscopy, adenoidal hypertrophy can usually be assessed on physical exam by assessing the quality of the voice. One’s voice becomes hyponasal (or termed nasal in lay speak) in quality when there is significant obstruction by the adenoids. In clinical practice, this can be assessed by asking the patient to say the name “Mickey Mouse” while pinching the nose and while not pinching the nose. If the adenoids are significantly enlarged, the Mickey Mouse phrase sounds the same, pinching or no pinching.

Enlarged adenoids can also lead to the typical “adenoid facies.” Adenoid facies can comprise open-mouth breathing, audible mouth breathing, and blueness around the lips and under the eyes (allergic shiners).

The use of the Mallampati score has recently come into vogue as a tool to judge airway obstruction. The Mallampati classification is an anesthesia tool used to describe the degree of overlap between the soft palate and the base of the tongue. Anesthesiologists use the score as an aid in predicting the degree of difficulty of intubation. The score is correlated with the presence of OSA. It is a scale from 1 to 4, with 4 describing severe overlap of the soft palate over the tongue base. While the published reports on OSA and Mallampati score describe an adult population, assessing a Mallampati score in kids is yet another clue that can be used in one’s assessment (Nuckton et al., 2006).

Visualization and auscultation of the chest can elicit clues to the diagnosis of OSA as well. If you look very carefully, one can oftentimes pick up a small pectus excavatum, which can suggest long-standing increased work of breathing during sleep. When a pectus excavatum is identified, one needs to determine if the patient was born with this chest wall deformity or whether it is acquired. When a pectus excavatum is present from birth and simply grows in parallel with the child’s growth, it is clinically insignificant. However, if the parents cannot remember it from birth, then it may have been acquired over time and might be an insidious sign of increased work of breathing during sleep.

Auscultation can sometimes be noteworthy for diminished breath sounds. Adenotonsillar hypertrophy can obstruct normal breathing such that the breath sounds are rendered less loud than you might expect.

Sometimes the most important element to the physical exam comes from just observing the child from afar. Sleepiness can be assessed if the child yawns a lot, seems unexpectedly quiet or withdrawn, or even falls asleep. Hyperactivity and impulsivity can manifest as the child bouncing all over the room, getting into things, and being poorly focused and poorly behaved. Fidgeting, leg bouncing, irritability, and tantrums are all easily observable and important to note. While all of these behaviors can of course be associated with normal childhood growth and development, over time, the skilled and experienced practitioner can begin to determine behaviors suggestive of excessive daytime sleepiness that stand out as abnormal. Furthermore, since sleep disorders of any cause (i.e., not just OSA) can masquerade as depression, anxiety, hyperactivity, or impulsivity, such global observations are of paramount importance.

OSA can have a major impact on growth; therefore, tracking height, weight, and body mass index need to be part of every office visit (Bonuck, Freeman, & Henderson, 2009). OSA can effect growth on both ends of the spectrum. In more severe cases, it can be associated with failure to thrive. In addition, it can be associated with insulin resistance and subsequent obesity (Gozal & Kheirandish-Gozal, 2009; Kohler, 2009; Spruyt et al., 2008).

When OSA has become long-standing and has begun to affect the cardiovascular system, there can be additional physical findings that become more obvious. Blood pressure can be elevated, and aberrant second heart sounds related to right heart strain can become pronounced (Sheldon et al., 2005).

DIAGNOSIS

The diagnosis of OSA has evolved over the years. Even though polysomnography (the overnight sleep study) remains the gold standard (Sheldon et al., 2005) for diagnosis, utilization and interpretation remains a challenge. If after evaluation the child is suspected of having OSA, he/she should ideally be referred for a sleep study. However, even when a child is referred, challenges exist. For example, many sleep labs do not study children and even fewer sleep labs study very young children and babies. Furthermore, the various monitoring devices involved with a sleep study can be frightening to children. Thus, when possible, it is preferred that the child is studied in a pediatric sleep lab staffed by pediatric trained sleep technicians. These pediatric trained technicians have the experience needed to get a child into the room, feel comfortable, engaged, and as willing a participant as possible.

The electrode leads are used to provide a complete assessment of cardiorespiratory, brain, and muscular physiology during sleep. Electroencephalogram leads assess brain wave activity and are designed to differentiate sleep stages and arousals. Their primary purpose is not to pick up seizure activity, but when obvious, epileptic activity can be seen.

Muscle activity is assessed by electromyogram leads placed on the chin and limbs. Muscular tone in the chin is a correlate for tone in the whole body and therefore can serve as an aid in distinguishing between stages of sleep. For example, there is nearly absent muscular tone during REM sleep; therefore, the chin lead will be silent during REM. The chin lead also becomes active during bruxism and lip-smacking.

Airflow can be assessed by an airflow pressure transducer at the nose and by oronasal thermistors at the nose and mouth. End tidal or transcutaneous CO₂ recording is often available and at times is invaluable in making the diagnosis of OSA.

Determination of chest and abdominal wall excursion allows one to gauge respiratory effort and to classify apneas as central or obstructive. Limb leads assess leg movements. Snore microphones assess snoring. Finally, real-time video is useful in observing sleep positions, restlessness, and seizures, and in verifying what may be unclear from the electrodes as seen on the computer monitor.

As extensive and cumbersome as this array of monitoring sounds and appears, it remains the gold standard for a variety of reasons. First of all, it has long been known that relying solely on history, audiotape or videotape, is insufficient for diagnosing OSA. Second, there are a variety of combinations and permutations using data from the full set of leads whereby a study can be judged positive and diagnostic for OSA. Additionally, OSA is frequently sleep stage specific (REM), and since REM is clustered in the latter half of the night, a full night’s monitoring is required. If one only performs an abbreviated study or a nap study, a majority of obstructive events might be missed. Finally, since OSA is but one reason (albeit very common) for restless and disturbed nighttime sleep, full polysomnography is as necessary to rule OSA in, as it is to rule other entities out.

Utilization of the sleep lab is also an issue of debate. As previously mentioned, in an ideal world with unlimited medical and financial resources, every child suspected of having OSA would have a sleep study. This, of course, is not an ideal world, and resources are limited as are skilled and trained personnel. The general guidelines for recommending a sleep study are as follows:

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