Contact WAO | e-News Sign Up | Site Map | Home  
World Allergy Organization
WAO's mission: To be a global resource and advocate in the field of allergy, advancing excellence in clinical care through education, research and training as a world-wide alliance of allergy and clinical immunology societies.

Upper Airway and Sleep Disorders in Adults

Richard J. Schwab, MD
University of Pennsylvania
Philadelphia, PA, USA

Goals

  • To understand and define the spectrum of sleep disordered breathing
  • To review the pathogenesis and clinical presentation of obstructive sleep apnea
  • To highlight the diagnostic algorithm in obstructive sleep apnea
  • To discuss medical consequences of obstructive sleep apnea

Spectrum of Sleep Disordered Breathing
Sleep disordered breathing should be considered a continuum of abnormality, i.e., a spectrum of diseases from snoring to UARS (upper airway resistance syndrome – snoring related arousals without reductions in airflow) to obstructive sleep apnea (combination of apneas {complete airway obstruction} and hypopneas {partial airway obstruction) to obesity-hypoventilation syndrome (Pickwickian syndrome):

Snoring < > UARS < > Hypopneas < > Obstructive Apneas < > Hypoventilation

Factors that can move individual patients down this spectrum include weight gain, increased age, sleep deprivation, alcohol (preferentially suppresses the activity of upper airway dilator muscles) and sedative use. Snoring should not be considered normal; it is often the first manifestation of sleep-disordered breathing.

Upper Airway Resistance Syndrome
The upper airway resistance is characterized by recurrent arousals secondary to increased upper airway resistance (or crescendo snoring). In this syndrome repeated arousals are noted secondary to snoring or increased upper airway resistance. These arousals may result in significant sleep fragmentation and daytime sleepiness. The upper airway resistance syndrome has also recently been associated with hypertension.

In order to accurately diagnose the upper airway resistance syndrome a polysomnogram with an esophageal balloon is necessary. Since most sleep laboratories do not use esophageal balloons a less invasive method of diagnosing the upper airway resistance syndrome is by counting arousals associated with episodes of snoring. It is likely, although unproven, that using snoring related arousals to diagnose the upper airway resistance syndrome underestimates the prevalence of this disorder. If the snoring related arousal index is > 5-10/hour, treatment should be considered for the upper airway resistance syndrome. The treatment of choice currently for the upper airway resistance syndrome is nasal CPAP although oral appliances and possibly upper airway surgery may be effective therapeutic interventions.

Epidemiology and Risk Factors for Obstructive Sleep Apnea
Sleep apnea is an extremely common disorder. The Wisconsin Sleep Cohort Study found that 9% of middle-aged males and 4% of middle-aged females had evidence for sleep apnea. If night-time and daytime symptoms (excessive sleepiness) were included in the definition of sleep apnea, 4% of middle-aged males and 2% of middle-aged females fulfilled this criterion. Epidemiological studies show a male predominance, i.e., obstructive sleep apnea is twice as common in males than females.

The major risk factor for obstructive sleep apnea, at least in adults, is obesity. Not surprisingly, it is fat in the neck that plays the largest role. In population studies, neck (or collar size) is the best predictor of the presence of sleep apnea. Approximately 30% of snoring males with a collar size > 17 inches will have obstructive sleep apnea. Neck size in women is less well investigated, but > 15 inches increases the risk for sleep apnea. Obesity is not the only risk factor for obstructive sleep apnea. Upper airway anatomy (enlargement of the tongue , tonsils (palatine and lingual), adenoids, soft palate, and lateral pharyngeal walls; and reduction in the size of the mandible /maxilla), genetic factors, endocrine disorders (hypothyroidism, acromegaly) and substances that reduce upper airway muscle tone (alcohol, sedatives or hypnotics) also play a role.

Clinical Presentation of Obstructive Sleep Apnea
Obstructive sleep apnea is not a difficult diagnosis to make and should be considered in all overweight or retrognathic (recessed jaw) patients who complain of habitual snoring and/or daytime sleepiness.

Symptoms
The cardinal symptoms of sleep apnea are excessive daytime sleepiness, sleep fragmentation and loud habitual snoring. Witnessed apneic episodes (nocturnal grunting/gasping) are frequently reported. Patients may fall asleep at inappropriate times, such as while watching television or reading, in the middle of a conversion, or while operating a motor vehicle. Patients with sleep apnea have a 3-7 fold greater rate of motor vehicle accidents than subjects without sleep apnea. Other common symptoms include personality changes (especially irritability), nocturia, morning headaches (this suggests hypercapnia and concomitant obesity-hypoventilation syndrome), intellectual impairment, reduction in libido, palpitations and memory loss.

Physical Examination
All patients with sleep apnea should have a careful head and neck examination paying particular attention to the size of the bony and soft tissue oropharyngeal structures. Neck size measured at the cricothyroid membrane should be obtained (>17 inches in men and >15 inches in women increases the risk for sleep apnea). Craniofacial risk factors for sleep apnea include retrognathia, micrognathia, a narrow hard palate, nasal obstruction, an overjet (greater than a 3 mm anterior-posterior distance between the upper and lower incisors during occlusion) and overbite (greater than a 3 mm vertical distance between the upper and lower incisors during occlusion). The nares should be examined for nasal polyps and nasal septal deviation. Retrognathia is defined as a > 0.5 cm retroposition of the gnathion (the most inferior point in the contour of the chin) relative to the plane of the nasion (the deepest point of the superior aspect of the nasal bone, i.e., the base of the nose). In general, the forehead, maxilla and mandible should be aligned; if the mandible is behind these structures, retrognathia is present. Upper airway soft tissue risk factors for sleep apnea include macroglossia, tonsillar hypertrophy (palantine or lingual) and enlargement of the soft palate/uvula and lateral pharyngeal walls. The tongue is considered enlarged if it is above the level of the mandibular occlusal plane. Tonsillar enlargement is defined as the presence of lateral impingement of greater than 50% of the posterior pharyngeal airspace. The uvula is considered enlarged if it is >1.5 cm in length or >1.0 cm in width. Lateral peritonsillar narrowing is defined as impingement of greater than 25% of the pharyngeal space by the peritonsillar tissues, excluding the tonsils. Recent studies using volumetric MRI have demonstrated enlargement of the tongue and lateral pharyngeal walls are important anatomic risk factors for sleep apnea. In addition, recent studies have demonstrated heritability and family aggregation of these upper airway anatomic risk factors for sleep apnea. Such data provide strong evidence for the genetic basis of sleep apnea.

Diagnosis of Obstructive Sleep Apnea
The gold standard for making the diagnosis of obstructive sleep apnea is with an overnight polysomnogram demonstrating recurrent episodes of cessation of respiration (apnea) or decrements in airflow (hypopneas) during sleep associated with arousals and arterial oxyhemoglobin desaturations. Patients with sleep apnea show respiratory effort (i.e., chest wall and abdominal wall movement), unlike patients with central sleep apnea in whom there is no respiratory drive. An apnea is defined as cessation of airflow for at least 10 seconds. An apnea can be obstructive (no airflow but continued respiratory effort), central (airflow and respiratory effort are both absent), or mixed. A mixed apnea is one which starts as a central event but then becomes obstructive during the same episode. Most patients with obstructive sleep apnea have both obstructive and mixed apneas. In addition, hypopneas (a decrement in airflow of 50% or more associated with a 4% fall in oxygen saturation and/or an electroencephalographic arousal) can produce similar clinical consequences as apneas. Therefore the apnea/hypopnea index (AHI: the number of apneas plus hypopneas per hour of sleep) has become the metric to define and quantitate the severity of obstructive sleep apnea. The apnea/hypopnea index is calculated from the number of apneas plus hypopneas per hour. An AHI of 0 - 5 events/hour is considered normal; an AHI 5 - 15 events/hour is considered mild sleep apnea; an AHI 15 - 30 events/ hour is considered moderate sleep apnea and an AHI > 30 events/hour is considered severe sleep apnea. In the hospitalized patient nocturnal oximetry demonstrating recurrent oxyhemoglobin desaturations has been used as a screening test for sleep apnea. During an apnea the PO2 will often decrease and the PCO2 will increase slightly.

Figure 1

Figure 1: Obstructive apneic episode in a patient with sleep apnea syndrome. The polysomnography traces from the top down are as follows: three EEG channels (C3-A2, C4-A2, OZ-A2); two EOG channels (R and L); submental EMG (EMG); right and left anterior tibialis EMG (RAT, LAT), electrocardiogram (EKG); nasal and oral airflow; chest and abdominal motion (chest & abd). During the apneic episodes, airflow is abnormal (both oral and nasal) with paradoxical motion of the rib cage and abdomen. At the end of the apneic episode, a burst of EMG activity occurs at the arousal. After arousal, respiration resumes with synchronous movements of the rib cage and abdomen.

Consequences of Obstructive Sleep Apnea
Consequences of obstructive sleep apnea can be broadly divided into those related to the excessive sleepiness and those related to the cardiovascular system. Excessive daytime sleepiness produces a number of different problems for patients with sleep apnea, among which the most serious is vehicular crashes. Studies in driving simulators indicate that sleep apnea impairs driving ability. Recently it has been demonstrated that patients with sleep apnea can be as impaired in driving skills as those who are over the legal blood alcohol concentration. Cardiovascular risks associated with sleep apnea include hypertension, myocardial infarction, cardiac arrhythmias and stroke. The sleep health heart study (6000 adults had sleep studies and were followed for cardiovascular morbidity) has demonstrated that patients with sleep apnea are at increased risk for hypertension. Obstructive sleep apnea has also been demonstrated to be an important risk factor for myocardial infarction and cerebral vascular accidents. Nocturnal cardiac arrhythmias including sinus bradycardia/tachycardia (most common arrhythmia), atrial fibrillation, atrial and ventricular tachycardia, heart block and sinus pauses have been reported during apneic episodes (the nocturnal arrhythmias are often a clue to the diagnosis). These arrhythmias often resolve with treatment of the obstructive sleep apnea so a pacemaker may not be indicated. Pulmonary hypertension and right heart failure develop in approximately 10 to 15% of patients with severe sleep apnea.

Slide Presentation