Obstructive sleep apnea (OSA) is a highly prevalent disorder typified by repeated episodes of complete or partial pharyngeal collapse and airway obstruction occurring during sleep. It is estimated by the seminal Wisconsin Sleep Cohort that OSA affects 3% of middle-aged women and 9% of middle-aged men, with incidence increasing in parallel with society’s worsening obesity rates. OSA is among the most common problems seen by Otolaryngologists and a recent NEJM (New England Journal of Medicine) editorial has described OSA as a “perioperative epidemic.”

The term sleep disordered breathing (SDB) refers to a large number of sleep-related breathing problems, of which OSA is just one, the others being beyond the scope of this chapter. In regards to obstructive diseases specifically, the severity can range from simple snoring to life-threatening obstruction. The more commonly employed terms are stated below.

Primary Snoring

Primary snoring is defined as snoring without concomitant arousals or sleep fragmentation. All patients with OSA will snore, but not all snorers have OSA. Although not pathological in and of itself, snoring can be associated with altered sleep habits (because of bed partner dissatisfaction). Additionally, there is emerging evidence that the physical trauma of the snoring vibrations on neck structures can be independently associated with carotid artery stenosis and stroke.

Upper Airway Resistance

Upper airway resistance remains poorly defined in the literature. It is generally accepted to consist of respiratory events during sleep that are not severe enough to qualify as apneas or hypopneas, but still lead to sleep fragmentation and daytime symptoms.

Obstructive Sleep Apnea

OSA is formally defined as repetitive episodes of airway obstruction consisting of either hypopneas (partial obstruction associated with hypoxia and brief sleep arousal) or apneas (complete obstruction for minimum of 10 seconds associated with hypoxia and brief arousal). In OSA evidence must also exist of respiratory effort being made in association with the decreased or absent airflow, in order to differentiate this from central sleep apnea (in which no respiratory efforts are made). Respiratory events in OSA are more common during stage 2 or rapid-eye-movement (REM) sleep, which in the adult are the largest proportional sleep stages.

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  Snoring

  
  
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  Witnessed choking or gasping

  
  
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  Frequent body moments

  
  
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  Disproportionate fatigue

  
  
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  Daytime somnolence

  
  
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  Morning headaches

  
  
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  Sensation of unrefreshing sleep

  
  
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  Memory loss

  
  
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  Sexual dysfunction

  
  
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  Personality changes

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  Increased odds-ratio of motor vehicle accidents (MVAs)

  
  
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  Loss of economic productivity

  
  
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  Workplace accidents

  
  
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  Patients with OSA are known to use more health-care resources

Hypertension

OSA is an independent risk factor for hypertension (HTN) development as shown by the Sleep Heart Health Study. This is thought to be associated with increased sympathetic tone from chronic hypoxia and the frequent cortical arousals. Once an apnea occurs, the cardiac output decreases, triggering increased firing of the sympathetic nervous system and associated increased systemic vascular resistance. This cycle happens repeatedly throughout the apneic sleep time and eventually persists throughout the day too. Successful treatment of OSA is known to decrease HTN severity even in patients resistant to pharmacotherapy.

Cardiovascular Disease

OSA is well known to be associated with increased risk of heart attack, stroke, and death. This has been prominently demonstrated in the Busselton Health Study, showing that untreated OSA was an independent mortality risk factor. OSA can also worsen preexisting congestive heart failure by decreasing cardiac output as well as altering catecholamine levels. Cardiac arrhythmias can also be seen in patients with OSA, with the most common being brady- or tachyarrhythmias.

Cerebrovascular Disease

Like the heart, the brain is also under hypoxic stress during OSA. In the midst of apneic events, there can be increases in the intracranial pressure leading to decreased cerebral perfusion, which correspondingly increases stroke risk. Additionally, the snoring associated with OSA can lead to atherosclerotic changes in the carotid arteries, worsening the chance of an embolic event in the brain.

History

Diagnosis begins with a thorough history. Patients should be questioned about sleep habits and hygiene, typical sleep initiation and wake-up times, and shift work, in addition to asking about the standard symptoms and signs of sleep apnea. History can also be used to distinguish fatigue from OSA versus other type of sleep disorders such as insomnia or simple lack of sleep. Comorbidities of OSA should be pursued. It is very important to question patients about their sleepiness at work or while driving, as in some jurisdictions or for certain occupations, the physician is required by law to notify the transportation authorities or company about excessively drowsy patients who are at risk of driving or operating equipment. If possible, a history should be taken from the bed partner, who can both corroborate and expand on the patient’s complaints. It is not surprising to find patients who claim to either be asymptomatic, or downplay their symptoms, as over years of untreated disease a process of normalization occurs. Screening tools can be also used to help quantify disease severity. The most commonly employed is the Epworth sleepiness scale (Figure 2-1), which is a validated measure of daytime somnolence (although not specific to OSA). A score over 10 is considered problematic. The Berlin scale is useful as a screening test for OSA as it is more specific, but is also more complex to employ. Quality-of-life scoring is valuable to assess the impact of disease on personal health. Performance vigilance testing is important as a direct measure of the impact of OSA on wakefulness—these tests are widely available on the Internet.

Physical Findings

All patients suspected of having OSA should undergo a complete head and neck examination to assess for areas of obstruction. The body mass index (BMI) should be calculated as well. Specific areas to examine include the following:

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  Nasal cavity

  
  
  
  
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    Deviated septum

    
    
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    Turbinate hypertrophy

    
    
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    Nasal polyposis

    
    
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    Concha bullosa

The nasal cavity should be examined both with a speculum and endoscope. If the nose is blocked, this can lead to downstream increases in airflow resistance both directly (by nasal obstruction) and secondarily (by forcing mouth opening which in turn drops the tongue and pushes the hyoid backward).

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  Nasopharynx

  
  
  
  
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    Adenoid tissue

  
  
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  Oral Cavity

  
  
  
  
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    Size and position of tongue

    
    
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    Scalloping of tongue edges

    
    
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    Mandibular or palatine tori

    
    
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    Assess occlusive status and jaw position

Scalloping of the tongue can indicate relative macroglossia. Jaw occlusion and position (Angle classification II in particular) should be noted as a retrognathic jaw, which means the tongue will be relatively posteriorly positioned. Tori of large size can also decrease room inside the oral cavity, which can in turn malposition the malleable tongue.

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  Oropharynx

  
  
  
  
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    Tonsil size and position

    
    
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    Soft palate thickness and position

    
    
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    Uvular size, wrinkles, thickness, and position

    
    
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    Medialized lateral pharyngeal walls

One of the most important physical assessments in OSA is the relationship between the tonsils, tongue, and palate. This can be graded using the Friedman staging system (Figure 2-2). The tonsils are Friedman graded from 0 to 4 as follows: 0 = no tonsil (prior tonsillectomy); 1 = small, lateral to the pillars; 2 = extend to edge of tonsil pillars; 3 = extend beyond tonsil pillars; 4 = hypertrophic and midline contact. The Friedman palate position grading differs from the anesthesiology Mallampati classification in that with the Friedman system the tongue is not protruded and remains in a neutral position with mouth open. The Friedman palate grades are as follows: I = posterior pharyngeal wall visible; II = uvula visible; III = soft palate visible; IV = hard palate visible. The Mallampati system is not correct to use when assessing OSA, as it is not an accurate reflection of the patient’s oropharyngeal anatomical relationships during sleep.

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  Hypopharynx

  
  
  
  
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    Size and position of tongue base relative to epiglottis

    
    
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    Lingual tonsil hypertrophy

The hypopharynx should be examined with a flexible fiberoptic endoscope to study both the retropalatal and retrolingual areas. The Mueller maneuver (MM) is a commonly employed test, during which the patient’s mouth is closed and nose pinched after which they are asked to inhale, and the examiner can see which areas of the pharynx collapse. This is done with the patient both sitting and lying down. MM is simple to perform and inexpensive but is hampered by poor inter- and intra-rater reliability. Additionally, there is a low correlation with intraoperative findings, and a low positive-predictive value for success at pharyngeal sleep surgery. Another valuable method of endoscopic assessment is to identify areas of obstruction seen in the pharynx at end expiration (which is thought to be the time of the respiration cycle most prone to collapse). This is a more reproducible maneuver and also more valid than the MM.

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  Supraglottis

  
  
  
  
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    Epiglottis shape

    
    
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    Epiglottis position relative to posterior pharyngeal wall

    
    
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    Size and position of tongue base relative to epiglottis