Signs and Symptoms of Obstructive Sleep Apnea and Upper Airway Resistance Syndrome


Obstructive Sleep Apnea

Obstructive sleep apnea (OSA) is characterized by repetitive episodes of complete or partial obstructions of the upper airway during sleep. The spectrum of these obstructive respiratory events during sleep occurs on a continuum ranging from hypopnea (reduced airflow during sleep) to apnea (complete airflow cessation during sleep). According to the International Classification of Sleep Disorders, 3rd edition, a diagnosis of OSA is defined as a Respiratory Disturbance Index (RDI) ≥5 with symptoms or an RDI ≥15 without symptoms. The severity of OSA is quantified by measuring the RDI, which includes the frequency of apneas (complete upper airway obstruction), hypopneas (partial upper airway obstruction), and arousals from sleep related to respiratory efforts ( Table 2.1 ).

Table 2.1
Symptoms of Obstructive Sleep Apnea
Sleep Symptoms Awake Symptoms
  • Snoring

  • Witnessed apneas

  • Choking/gasping

  • Restless sleep/ frequent arousals

  • Bruxism

  • Gastroesophageal reflux

  • Nocturia

  • Excessive daytime sleepiness

  • Morning headache

  • Neurocognitive impairment

  • Vigilance

  • Executive function

  • Motor coordination

  • Mood and personality changes

  • Depression

  • Anxiety

  • Sexual dysfunction

In the general adult population, the prevalence of OSA defined by ≥5 apnea and hypopnea events per hour of sleep associated with excessive sleepiness is approximately 3% to 7% in men and 2% to 5% in women. The prevalence of OSA is much higher in patients with cardiac or metabolic disorders than in the general population. The incidence has been much less studied than its prevalence. A longitudinal cohort study of US communities (2968 men and women, mean age ± SD 62.1 ± 9.9 years) assessed sleep-disordered breathing (SDB) at two time points that were 5 years apart. Over the 5-year period, the overall incidence of moderate to severe OSA, defined by an Apnea/Hypopnea Index (AHI) >15, was 11.1% in men and 4.9% in women.

Risk factors for OSA include obesity (the greatest risk factor), upper airway abnormalities, male gender, menopause, and age. The prevalence of OSA associated with a higher risk of morbidity and mortality increases with age and peaks at approximately 55 years of age. Sex differences in the incidence of OSA remain significant after adjusting for confounding variables. Weight change is a critical factor for the progression of the disease; however, OSA may progress over time even in those with stable weight.

Clinical Presentation of OSA

Sleep-Related (Nocturnal) Symptoms

Snoring

Snoring is a fluttering sound created by the vibrations of pharyngeal tissues during sleep, which is a ubiquitous complaint of bed partners worldwide and leads to many patient requests for treatment recommendations. Most authors support a continuum of snoring from simple snoring through upper airway resistance syndrome (UARS) and to various degrees of OSA. Patients who snore but have an AHI <5 tend to be classified as primary or habitual snorers, but may fall in the category of UARS patients. Although the prevalence of snoring varies between studies because of its highly subjective nature, its prevalence has been reported as 5% to 78% in males and 2% to 59% in females. The gender difference is perhaps not surprising given that being male is one of the risk factors for snoring. This is highlighted in one of the few meta-analyses in the epidemiology of snoring. In addition to gender, sleep positions affect snoring such that supine positions are associated with more snoring and apneas than lateral sleeping positions.

Witnessed Apneas and Nocturnal Choking/Gasping

Witnessed apneas and nocturnal choking are related to apneic events and are the second most common nocturnal symptom reported in OSA. Up to 75% of OSA patients' bed partners report witnessed apneas. Patients themselves are rarely aware of the apneas. Nocturnal choking or gasping, sometimes described by patients as a sensation of suffocation, has been observed in 18% to 31% of patients with OSA. These episodes typically occur with arousals, are associated with feelings of panic and anxiety, and generally subside within a few seconds. During apneas or hypopneas, greater negative intrathoracic pressures are generated as patients increase their inspiration efforts to overcome the upper airway obstruction. This increases venous return to the heart and thus elevates pulmonary capillary wedge pressure, which produces the sensation of dyspnea. Nocturnal choking or gasping is the more reliable indicator of OSA compared with snoring. However, choking or gasping from OSA must be differentiated from other causes of nocturnal breathlessness such as gastroesophageal reflux (GER) paroxysmal nocturnal dyspnea in patients with left ventricular failure, nocturnal asthma, or Cheyne–Stokes respiration ( Table 2.2 ).

Table 2.2
Physical Signs of OSA
Anthropometric Measurements
  • Obesity (body mass index)

  • Neck circumference (>40 cm)

Craniofacial Structure Evaluation
  • High, narrow arched palate

  • Retrognathia

  • Overjet/Overbite

  • Malocclusion

  • Bruxism (teeth grinding)

Nasal Cavity, Oral Cavity, and Pharyngeal Examination
Nasal Cavity
  • Inspiration collapse of nasal valve

  • Septal deviation

  • Inferior turbinate hypertrophy

Oral Cavity and Pharynx
  • Short lingual frenulum

  • Macroglossia (scalloping of tongue border)

  • Redundant and low-lying soft palate

  • Elongated uvula

  • Tonsil hypertrophy

Flexible Nasopharyngoscopy With Mueller Maneuver
  • Adenoid hypertrophy

  • Narrowing of retropalatal and retroglossal space

  • Collapse of lateral pharyngeal wall

Sleep Bruxism

Sleep bruxism is defined as a stereotyped movement disorder occurring during sleep and is characterized by teeth grinding and clenching, which is also a common finding in OSA patients. There is a positive correlation between the frequency of OSA and sleep bruxism events in OSA patients.

However, sleep bruxism is not directly dependent on apneic episodes but rather seems to be related to sleep disruption and arousal, which is influenced by sympathetic/parasympathetic fluctuations during sleep. It was observed that there is a rise in autonomic sympathetic cardiac activity before bruxism with increasing brain activity, heart rate, suprahyoid muscle tone, amplitude of respiration, and masseter and temporalis muscle activity. The bruxism episodes are followed by activation of the parasympathetic system with bradycardia, hypersalivation, and increased patency of the upper airways. It is also known that due to arousals and hypoxia, the sympathetic nervous system is activated. It is possible that sleep bruxism is part of the arousal process in which respiratory disturbances, leading to sleep fragmentation and arousals, trigger the muscles of the masticatory organ to restore normal breathing. Continuous positive airway pressure (CPAP) alone could eliminate sleep bruxism episodes in OSA patients whose episodes parallel arousal responses. Because the presence of sleep bruxism could represent a contraindication for the use of oral appliances in the treatment of OSA, CPAP treatment may be preferred.

Gastroesophageal Reflux

The prevalence of GER has been reported in 58% to 62% of patients with OSA. However, GER and OSA share several risk factors, which are both confounded by obesity. Apneas may increase respiratory effort, thereby increasing transdiaphragmatic pressure and decreasing intrathoracic pressure, eventually facilitating the retrograde movement of the gastric contents into the esophagus. However, some studies have failed to show a significant relationship between GER and OSA. Although the relationship between the two is not clear, treatment of OSA has been shown to improve GER, and CPAP has been demonstrated to reduce the total 24-hour esophageal acid contact time.

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