Obstructive Sleep Apnea

Article Author:
Jennifer Slowik
Article Editor:
Jacob Collen
6/7/2020 12:26:43 PM
PubMed Link:
Obstructive Sleep Apnea


Obstructive sleep apnea (OSA) is characterized by episodes of complete or partial collapse of the airway with an associated decrease in oxygen saturation or arousal from sleep. This disturbance results in fragmented, nonrestorative sleep. Other symptoms include loud, disruptive snoring, witnessed apneas during sleep, and excessive daytime sleepiness. OSA has significant implications for cardiovascular health, mental illness, quality of life and driving safety.[1][2][3]

OSA is associated with daytime somnolence and affects millions of people. The apneic episodes may occur hundreds of times each night and are associated with alterations in heart rate, drop in oxygen saturation and loud breathing sounds. The disorder is associated with very high morbidity and mortality including hypertension, coronary artery disease, depression, insulin-resistant diabetes, and sleep-related accidents.


Sleep apnea occurs when there is not enough space to accommodate sufficient airflow in a portion of the upper airway during sleep. When muscle tone is decreased, the result is a repetitive total or partial collapse of the airway. In children, the most common cause of obstructive sleep apnea is enlarged tonsils and/or adenoids. In adults, it is most commonly associated with obesity, male sex, and advancing age.

Structural factors associated with OSA include:

  • Micrognathia, retrognathia
  • Facial elongation
  • Mandibular hypoplasia
  • Adenoid and tonsillar hypertrophy
  • Down syndrome
  • Prader Willi syndrome
  • Inferior displacement of the hyoid

Nonanatomic risk factors include:

  • Central fat distribution
  • Obesity
  • Advanced age
  • Male gender
  • Alcohol use
  • Smoking
  • Use of sedatives
  • Supine sleeping position
  • Habitual snoring

Medical disorders associated with OSA include:

  • Stroke
  • Hypothyroidism
  • Metabolic syndrome
  • Acromegaly
  • Neurological disorders (eg myasthenia gravis)


In the United States, it has been reported that 4% of men and 2% of women meet criteria for obstructive sleep apnea. More recently, prevalence has been reported to be as high as 14% of men and 5% of women in the United States. Prevalence is higher in Hispanic, African American, and Asian populations. Prevalence also increases with age, and when individuals reach 50 years of age or more, there are as many women as men who develop the disorder.


Muscle tone decreases during sleep and is lowest during REM sleep. An episode of apnea in obstructive sleep apnea is caused by at least 90% anterior to a posterior collapse of the airway for more than 10 seconds. A hypopnea is characterized by at least 30% reduction in airflow for more than 10 seconds associated with an oxygen desaturation or arousal on electroencephalogram (EEG).

The majority of patients with OSA have upper airway obstruction either at the level of the tongue or the soft palate. Other anatomical factors that contribute to OSA include enlarged tonsils, large volume of the tongue, abnormal maxilla position, length of the soft palate and a decrease in the cross sectional area of the upper airways.

The apneic episodes tend to occur in clusters with oxygen desaturation.

History and Physical

The typical adult obstructive sleep apnea patient is overweight or obese middle-aged male or postmenopausal female with excessive daytime sleepiness and loud nightly snoring. They may also complain of waking to gasp for breath or choking, sleep maintenance insomnia, night sweats, nighttime reflux, and nocturia in the absence of excessive nighttime liquid intake. A physical exam is typically notable for a larger than average neck circumference (17 inches in males) with crowded oropharynx (Mallampati 3 to 4) and large tongue. Retrognathism may be present. Patients with refractory atrial fibrillation, resistant hypertension, and history of a stroke should be screened for sleep apnea regardless of symptoms.

The typical child with obstructive sleep apnea will have loud nightly snoring, may be hyperactive rather than sleepy, and may have academic difficulties. These children can be incorrectly diagnosed with attention deficit hyperactivity disorder (ADHD). Night sweats, nighttime reflux, sleep maintenance insomnia, restless sleep with frequent limb movements, and secondary nocturnal enuresis may also be present. A physical exam is often notable for adenoidal facies, tonsillar hypertrophy, hyponasal speech, and high arched palate. Patients with Down syndrome and any other condition associated with hypotonia should be screened for obstructive sleep apnea regardless of symptoms.

The Epworth Sleepiness Scale can be used to gauge the patient's likelihood of dozing in different settings as an indicator of inadequate restorative nighttime sleep. The score ranges from zero to 24, and more than ten is suggestive of a sleep disorder rather than generalized fatigue. More specific to obstructive sleep apnea is the STOP-BANG score. (S) snoring, (T) tired, (O) observed apnea, (P) pressure (blood pressure), (B) BMI more than 35, (A) older than 50 years old, (N) neck greater than 40 cm, and (G) gender (male). If there are three or more positive answers, the patient is considered high risk of obstructive sleep apnea and should be referred for further evaluation. There is a modified STOP-BANG questionnaire for older children and teens (nine to 17 years old) that allows parents to report how often the child snores loudly or has witnessed apneas and assesses for additional risk factors (presence of hypertension, obesity, neck circumference more than 95 percentile for age, male sex). Alternatively, the Berlin Questionnaire evaluates the presence, loudness, and frequency of snoring, the presence of apneas, daytime sleepiness, hypertension, and obesity to predict a high or low likelihood of sleep apnea.


Nighttime in-laboratory Level 1 polysomnography (PSG) is the standard gold test for diagnosis of obstructive sleep apnea. During the test, patients are monitored with EEG leads, pulse oximetry, temperature and pressure sensors to detect nasal and oral airflow, respiratory impedance plethysmography or similar resistance belts around the chest and abdomen to detect motion, an ECG lead, and EMG sensors to detect muscle contraction in the chin, chest, and legs. A hypopnea can be based on one of two criteria. It can either be a reduction in airflow of at least 30% for more than 10 seconds associated with at least 4% oxygen desaturation or a reduction in airflow of at least 30% for more than 10 seconds associated with at least 3% oxygen desaturation or an arousal from sleep on EEG.

Home sleep tests (HST) have gained popularity due to their relative accessibility and lower cost. They are appropriate for adults with a high pretest probability for sleep apnea and no significant medical comorbidities (advanced congestive heart failure, COPD, and neurologic disorders). These are level 3 sleep tests consisting of pulse oximetry, heart rate monitoring, temperature and pressure sensors to detect nasal and oral airflow, resistance belts around the chest and abdomen to detect motion, and a sensor to detect body position. Moderate and severe sleep apnea is detected on these tests, but due to the chance of underestimating the apnea-hypopnea index (AHI) relative to the total recording time (which may be longer than the total sleep time measured on an in-lab study), mild sleep apnea may go undiagnosed, and a repeat in-lab study may be needed.

The apnea-hypopnea index is the average number of obstructive event per hour. In adults, if the apnea-hypopnea index is greater than or equal to fifteen events per hour the diagnosis of obstructive sleep apnea is made with 15 to 29.9 per hour being moderate, and 30 or more events per hour being severe obstructive sleep apnea. An apnea-hypopnea index 5 to 14.9/hour is considered mild obstructive sleep apnea but only if there are clinical sequelae of the condition reported (excessive daytime sleepiness, sleep maintenance insomnia, cognitive dysfunction). Children are diagnosed with mild obstructive sleep apnea with an apnea-hypopnea index 1 to 4.9 per hour and clinical sequelae. Apnea-hypopnea index 5 to 9.9 events per hour is moderate and 10 or greater per hour is severe. Either adult or child criteria can be used for patients 13 to 17 years old at the discretion of the clinician depending on the clinical picture.[4][5][6]

Treatment / Management

For adults, the use of continuous positive airway pressure (CPAP) is the most effective treatment, and diligent adherence to nightly CPAP use can result in near complete resolution of symptoms. For patients unable or unwilling to use CPAP or those who will be unable to access electricity reliably, custom fitted and titrated oral appliances can be used to bring the lower jaw forward and relieve airway obstruction. This typically works best for candidates deemed to have appropriate dentition and mild to moderate sleep apnea. Severe obstructive sleep apnea can be treated with BiPAP as well and is better tolerated by patients who require higher pressure settings (greater than 15 cm to 20 cm H2O). For all patients, it is important to address any concomitant nasal obstruction with nasal steroids for allergic rhinitis or surgically for nasal valve collapse.

For obstructive sleep apnea with a strong positional component, a positioning device to keep a patient on his or her side can be an option. Although weight loss is recommended and can often decrease the severity of obstructive sleep apnea, it is not usually curative by itself.  

The primary treatment for obstructive sleep apnea in a child is tonsillectomy and adenoidectomy. The consideration for surgery should be balanced with the severity of symptoms, physical exam, and age. In mild cases, a trial of montelukast and nasal steroids may be enough to reduce the apnea-hypopnea index to goal. There are surgical options for adults, but these are usually reserved for severe obstructive sleep apnea and patients unable to tolerate noninvasive treatment modalities due to surgical risks and varying efficacy.

Uvulopalatopharyngoplasty (UPPP) is a term used to describe surgically removing the uvula and tissue from the soft palate to create more space in the oropharynx. This is sometimes done in conjunction with a tonsillectomy and adenoidectomy. More recently, drug-induced sleep endoscopy (DISE) has been used for preoperative planning to identify multiples levels of obstruction that are often present in these patients. This allows surgeons to address any nasal, soft palate and hypopharyngeal obstructions that may be present during a single surgery.

Another surgical option is maxillomandibular advancement (MMA) in which both the upper and lower jaws are detached and surgically advanced anteriorly to increase space in the oropharynx. This is best for patients with retrognathia and is less successful in older patients or those with larger neck circumferences.

A newer option is the implantable hypoglossal nerve stimulator. It works by stimulating the genioglossus (upper airway dilator muscle) during apneas resulting in protrusion of the tongue and relief of the obstruction. To be considered a candidate patient must meet the following criteria: BMI  less than 32, more than 22 years of age, apnea-hypopnea index 2 to 65 with less than 25% central apneas, unable to tolerate CPAP and no complete concentric collapse at the palate on drug induced sleep endoscopy.  The use of a permanent surgically-implanted device with limited time on the market and limited published long-term data on safety and efficacy should be pursued in specialty centers with experience in the surgical treatment of sleep-disordered breathing, in appropriately selected patients.

In extreme cases, obstructive sleep apnea can also be treated with a tracheostomy to bypass the oropharyngeal obstruction. This management option is also best addressed at academic or specialty sleep centers that are experienced in the care of patients with tracheostomy.  Such patients will encounter numerous challenges with home care and durable medical equipment and family/partner education on tracheostomy management. Many patients with severe sleep disordered breathing requiring tracheostomy have comorbidities and require long term home-based mechanical ventilation, the management of which will be outside the scope of most community sleep medicine practices.

Patients should be counseled to avoid alcohol, benzodiazepines, opiates, and some antidepressants which may worsen their condition.  Most importantly, patients should reflect on the impact of sleep duration and their health, and place a priority on getting at least 7 to 8 hours of sleep per night. No treatment for OSA per se will correct insufficient sleep.[7][8][9]

Differential Diagnosis

  • Asthma
  • Central sleep apnea
  • Chronic Obstructive Pulmonary Disease
  • Depression
  • Gastroesophageal reflux
  • Hypothyroidism
  • Narcolepsy
  • Periodic limb movement disorder


The short term prognosis with treatment is good but the long term prognosis is guarded. The biggest problem is the lack of compliance with CPAP. Almost 50% of patients stop using CPAP within the first month. Many patients are at risk for adverse cardiac events and stroke. Those patients who do use CPAP regularly do have improved survival compared to those who do not. Further, OSA is also associated with pulmonary hypertension, hypercapnia, hypoxemia, and daytime sedation. In addition, there is a high risk of motor vehicle accidents in these individuals. The overall life expectancy of patients with OSA is lower than the general population.

Enhancing Healthcare Team Outcomes

The management of patients with OSA is with an interprofessional team that includes a sleep specialist, internist, cardiologist, ENT surgeon, dietitian, pulmonologist and neurologist. There are many options to treat OSA of which the primary one is CPAP. Unfortunately, compliance with CPAP remains low. Some patients may benefit from an oral or nasal device but again compliance remains an issue. Surgery is the last step and should only be considered after a thorough evaluation of the patient. Surgery does not cure the disorder, is expensive and associated with serious complications. The prognosis for most patients with OSA is guarded. Until the patient starts to lose weight, most therapies have poor efficacy.


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