eMedicine Specialties > Pulmonology > Sleep-Related Disorders

Obstructive Sleep Apnea

Author: Ralph Downey III, PhD, DABSM, FAASM, Associate Professor of Medicine, Pediatrics, and Neurology, Loma University School of Medicine; Adjunct Associate Professor, Department of Psychology, University of California at Riverside; Chief, Sleep Medicine, Loma Linda University Medical Center and the Loma Linda University Children's Hospital
Coauthor(s): Philip M Gold, MD, Professor of Medicine, Chief of Pulmonary and Critical Care Medicine, Medical Director of Respiratory Care, Loma Linda University Medical Center; Himanshu Wickramasinghe, MD, MBBS, Attending Physician; Pulmonary, Critical Care, and Sleep Medicine; Henry Mayo Newhall Memorial Hospital, Valencia, California
Contributor Information and Disclosures

Updated: Jul 30, 2009

Introduction

Background

Obstructive sleep apnea (OSA) is a sleep disorder that involves cessation or significant decrease in airflow in the presence of breathing effort. OSA is a sleep disorder characterized by recurrent episodes of upper airway (UA) collapse during sleep.¹ By definition, apnea episodes last 10 seconds or longer and commonly last 30 seconds or longer. Apnea may occur hundreds of times nightly, 1-2 times per minute in severe OSA patients, and is often accompanied by wide swings in heart rate, precipitous decrease in oxygen saturation, and brief electroencephalogram (EEG) arousals concomitant with stertorous breathing sounds as a bolus of air is exhaled when the airway reopens. This may occur hundreds of times nightly. Obstructive apnea events are most often associated with recurrent sleep arousals and recurrent oxygen desaturation.

Three cardinal symptoms of sleep apnea include snoring, sleepiness, and significant-other report of sleep apnea episodes. This 3 S alliteration is a helpful mnemonic to busy clinicians in assessing patients for OSA. It has proven to be valuable in teaching residents to be sensitive in the identification and appropriate referral of these patients for further study Also helpful is if the patient’s spouse or someone close to him or her can attend the visit because often the sleeper is unaware he or she has OSA, and, in fact, he or she may regard themselves as "a good sleeper" because they "can sleep anytime, anywhere" (eg, waiting in the physician’s, in traffic, in class, at his or her office) Sleepiness is one of the potentially most morbid symptoms of sleep apnea, owing to the accidents that can occur as a result of it.

OSA is a very important diagnosis for physicians to consider because of its strong association with and potential cause of the most debilitating medical conditions, including hypertension, cardiovascular disease, coronary artery disease, insulin-resistance diabetes, depression, and, as mentioned, sleepiness-related accidents, which are discussed in greater detail in Mortality/Morbidity and Medicolegal Pitfalls.

OSA is an increasingly prevalent condition, in both adults and children, in modern society.  Approximately 24% of men and 9% of women have OSA, with and without excessive daytime sleepiness.² The prevalence in children is less certain, but an increasingly large segment of the adolescent population is seen in the author’s sleep center who are often obese and present similar to many of their adult counterparts, with one important exception: they may be sleepy and/or hyperactive. A 2007 study has suggested that approximately 6% of adolescents have weekly sleep-related disordered breathing.³ Also see Obstructive Sleep Apnea Syndrome in eMedicine’s Pediatrics section.

OSA should be diagnosed and treated promptly. OSA can be reversed quickly with the appropriate titration of continuous positive airway pressure (CPAP) devices. CPAP is the standard treatment option for OSA.

A sleep-related disordered breathing (SRDB) continuum has been described and is supported by research.⁴ The SRDB continuum suggests that snoring is the initial presenting symptom, and it increases in severity over time and it increases in association with medical disorders that may serve to exacerbate the disorder, such as obesity. Snoring has a constellation of pathophysiological effects⁵ ; as the disease progresses SRBD patients begin to develop increased UA resistance that results in a new hallmark symptom: sleepiness. Sleepiness is caused by increased arousals from sleep.⁶ This syndrome has been described as the UA resistance syndrome (UARS).

Before OSA with residual daytime sleepiness is considered and treated, it is important to know if the pressure is indeed ideal. The author’s approach is to be able to conclusively demonstrate that CPAP has effectively eliminate snoring, UARS, and OSA in the supine position and in rapid eye movement (REM) sleep, 2 sleep states during which SRDB is worsened. Sometimes, a single-night CPAP titration study is not sufficient to make this conclusion. Data suggest that the author’s sleep center titration under titrates an average of 2 cm water.¹ Based on these data, some may increase the CPAP pressure by 2 cm water. If the empirical increase does not effectively treat the EDS, then a PSG with a CPAP titration in the sleep disorders center is warranted to adjust the pressure while the patient is in the supine position and in REM sleep so that snoring, UARS, and OSA are eliminated.

If these steps have been taken, then performing a multiple sleep latency test (MSLT) is reasonable in order to (1) verify objective daytime sleepiness compared with the subjective sleepiness of the Epworth Sleepiness Scale (ESS), because the correlation is low (r = 0.34) and(2) exclude other sleep disorders known to have hypersomnia as a major presenting symptom (eg, insufficient sleep syndrome, narcolepsy), because insufficient sleep syndrome is the most common cause of hypersomnia and OSA is more common among patients who have narcolepsy (a 30% incidence rate vs 1-4% in the population).

The description of a continuum may have first been described by Elio Lugaresi, an Italian Sleep Specialist, during a 1987 Association for the Psychophysiological Study of Sleep presentation in Copenhagen, Denmark). Dr Lugaresi used the term "heavy snorers disease" to articulate the SRDB continuum. He made the argument that snoring is the beginning of the so-called heavy snorers disease. He presented data showing that the earlier snoring occurred in adult life, the more severe the obstructive apnea would be later, and OSA presented earlier in life.

Historical perspectives

The history of the discovery of sleep apnea is interesting and is the topic of a paper published in 2008.⁷

In literature, Charles Dickens has been credited with one of the first descriptions in print regarding sleep apnea when he wrote of "Sleepy Joe," an obese man who sat in the corner of an English pub asleep. The archetype of a rotund, sleepy man became eponymous with "pickwickian syndrome" by Burwell in 1956.⁸ The prevailing belief at the time was that "pickwickians" had breathing disorders and drowsiness due to "carbon dioxide poisoning."

A number of individuals have played important roles in advancing sleep science to the point that we have come to understand OSA. Detailing the history of OSA is beyond the scope of this article; however, a few highlights are mentioned.

Gestaut, Tassinari, and Duron⁹ in France and Jung and Kuhlo¹⁰ in Germany provided perhaps the most accurate descriptions of OSA at about the same time, in 1965.

The first known successful treatment for OSA was tracheostomy in 1970 by Elio Lugaresi and colleagues at the University of Bologna in Italy. A primary reason a tracheostomy was important to the understanding of OSA is that performing the tracheostomy left little doubt that OSA was due to an obstructed UA, and not due to a dysfunction of the brain’s respiratory centers. The elevated blood pressure in these patients was of grave concern to Dr Lugaresi, and post-tracheostomy the blood pressure dropped substantially. For the next 11-16 years, tracheostomy and weight loss were the only established beneficial remedies for OSA

In 1981, Sullivan et al introduced CPAP as a treatment for OSA.¹¹ It quickly gained worldwide acceptance by 1986, and it replaced tracheostomy as the most useful and desirable treatment. As is often the case in history, it is perplexing how such a simple device introduced so long ago can transform modern medicine in ways not sooner foreseen. CPAP was a tremendous advance for thousands of OSA patients who needed care and for clinicians who would soon solely specialize in sleep medicine.

Around the time when CPAP was introduced, corrective surgery was introduced and would become the forerunner of further developments in the field of sleep medicine. In 1981, Fugita and colleagues introduced uvulopalatopharyngoplasty (UPPP).¹²

Other treatments, including oral appliance (OA) therapy, are also now treatment alternatives for OSA. Future advances in these and other therapies (eg, stimulation of the genioglossus muscle) are exciting. As was the case with CPAP, the simplest procedure, mechanical device, or drug may astound the medical community by providing the next revolution in the treatment of OSA. For a complete and elegant description of the history of sleep medicine, see Principles and Practice of Sleep Medicine.¹³

Definition

According to the American Academy of Sleep Medicine (AASM) International Classification of Sleep Disorders: Diagnostic and Coding Manual, Second Edition,¹⁴ OSA is characterized by repetitive episodes of complete (apnea) or partial (hypopnea) UA obstruction occurring during sleep. By definition, apneic and hypopneic events last a minimum of 10 seconds. At least 5 apnea events must occur per hour of sleep time in association with clinical symptoms, or at least 15 apnea events must occur per hour of sleep time with or without clinical symptoms.

Pathophysiology

Available evidence indicates that pharyngeal collapse is responsible for the recurrent UA obstruction during sleep in patients with OSA.

UA size and shape

During wakefulness, the pharyngeal airway appears to be smaller in patients with OSA compared with healthy subjects. In the absence of craniofacial abnormalities, the soft palate, tongue, parapharyngeal fat pads, and lateral pharyngeal walls are enlarged.

Changes in transmural pressure in the UA

Transmural pressure is the difference between intraluminal pressure and the surrounding tissue pressure. If transmural pressure decreases, the cross-sectional area of the pharynx decreases. If this pressure passes a critical point, pharyngeal closing pressure is reached. OSA occurs when the net forces reach the closing pressure.

Risk factors for OSA

Static factors and dynamic factors increase the risk of OSA. Static factors include surface adhesive forces, neck and jaw posture, tracheal tug, and gravity. Gravitational forces are felt simply by tilting one's head back to where the retroposition of the tongue and soft palate reduce the pharyngeal space. For most patients, OSA worsens in the supine sleeping position.

Dynamic factors include nasal and pharyngeal airway resistance, the Bernoulli effect, and dynamic compliance.

Any anatomic feature that decreases the size of the pharynx increases the likelihood of OSA. One example of this effect is retrognathia. Dr Robin was the first to work on a mandibular-advancement device to help patients with what became known as Pierre Robin syndrome or Robin syndrome. His patients benefitted because protrusion of the mandible increased the cross-sectional area of the pharynx, among other effects.

The Bernoulli effect plays an important dynamic role in OSA pathophysiology. In accordance with this effect, airflow velocity increases at the site of stricture in the airway. As airway velocity increases, pressure on the lateral wall decreases. If the transmural closing pressure is reached, the airway collapses. The Bernoulli effect is exaggerated in areas where the airway is most compliant. Loads on the pharyngeal walls increase compliance and, hence, increase the likelihood of collapse.

This effect helps to partially explain why obese patients, and particularly those with fat deposition in the neck, are most likely to have OSA. Moreover, the cross-sectional area of the airway in patients with OSA is smaller than that of people without OSA; this difference is due to the volume of the soft tissue, including the tongue, lateral pharyngeal walls, soft palate, and parapharyngeal fat pads. In one study, the increased volume of these areas was independent of sex, age, ethnicity, craniofacial size, and fat deposition surrounding the UA.¹⁵

Given these principles, the reasons why the likelihood of OSA is increased among obese patients, why weight loss decreases the risk of OSA, and why physical examination helps in predicting the presence of OSA are understandable. However, the clinical situation is complex because of the interplay of known static and dynamic factors and because of unknown factors. Data do not explain why sex, age, and ethnicity are not evenly distributed across epidemiologic studies of OSA patients. Furthermore, data or physical findings are not helpful for determining with precision who will or will not have OSA and who can or who cannot be cured with UA surgery.

Frequency

United States

Although early investigators estimated the prevalence of sleep-disordered breathing (SDB) to be 2% for middle-aged women and 4% for middle-aged men, more recent research indicates a prevalence of 4% for women and 9% for men.²

The National Commission on Sleep Disorders Research estimated that minimal SDB (respiratory disturbance index [RDI] >5) affects 7-18 million people in the United States and that relatively severe cases (RDI >15) affect 1.8-4 million people. The prevalence increases with age. SDB remains undiagnosed in approximately 92% of affected women and 80% of affected men.

Mortality/Morbidity

In clinical practice, little doubt exists that sleep apnea can affect a person's quality of life in many ways. Sleep apnea is now known to be a public health hazard because of accidents due to sleepiness. Moreover, patients often have hypoxemia with each apneic event, and profound and repetitive hypoxia can affect end organ systems.

Excessive daytime sleepiness

EDS is one of the most common and difficult symptoms clinicians treat in patients with OSA. Patients do not always accurately describe their sleepiness on the ESS compared with objective measures. Nonetheless, EDS is one of the most debilitating symptoms because it reduces quality of life, it impairs daytime performance, and it causes neurocognitive deficits (eg, memory deficits).

Although CPAP quickly reverses EDS in most patients, not all patients use CPAP. Moreover, some patients remain sleepy despite effective CPAP. In these patients, modafinil at 200-400 mg/d can effectively enhance alertness without changing CPAP use.¹⁶ Patients with residual excessive sleepiness despite effective CPAP use are an interesting subgroup of patients. The mechanism of EDS in these patients awaits further study.

Partly because of their EDS, daytime functioning, intellectual capacity, memory, psychomotor vigilance (decreased attention and concentration), and motor coordination are substantially impaired in patients with OSA. Causes include both sleep fragmentation and hypoxemia due to OSA. Whether these causes can be reversed awaits further study.

Patients with OSA have more automobile accidents than people without OSA. Determining which OSA patients are likely to have an accident is unpredictable from the existing data.

Patients with OSA do not perform as well as healthy control subjects during driving simulation tests, but their performance may return to normal after treatment. Therefore, access to effective treatment is a pivotal concern in sleep medicine.

Cardiovascular

A Scientific Statement was published by the American Heart Association and the American College of Cardiology Foundation on August 25, 2008. This expert review examined OSA and cardiovascular disease. The results are paraphrased below.¹⁷

The possible mechanisms through which OSA may lead to cardiovascular disease were examined. OSA patients often have hypoxemia, reoxygenation, sleep arousals, less sleep time than healthy individuals, elevated negative intrathoracic pressure, and, in some individuals, hypercapnia. The commonly accepted contributions of these OSA-related pathophysiological factors may affect sympathetic activation, metabolic dysregulation, left atrial enlargement, endothelial dysfunction, systemic inflammation, and hypercoagulability. These mechanisms can lead to hypertension (both systemic and pulmonary), heart failure, cardiac arrhythmias, renal disease, stroke and myocardial infarction, and sudden death in sleep.

Two of the most significant findings from the Somers et al¹⁷ review are (1) that the data suggest that evaluation and treatment for OSA is not recommended in every patient with cardiac disease, but the threshold for a referral for a PSG study and for treatment of OSA should be low and (2) because OSA affects younger individuals with cardiovascular disease to a greater extent than older individuals with cardiovascular disease, this threshold for OSA evaluation and treatment should be even lower.

Other significant findings from the review are as follows¹⁷ :

• Hypertension: All-cause mortality rates are higher individuals with blunted or absent decrease in nighttime blood pressure. Additionally, CPAP treatment was shown to have moderate and variable effects on blood pressure in OSA patients.¹⁸ Further, antihypertensive drug treatment does not improve OSA; however, clonidine, which is a REM sleep suppressant, may improve OSA by reducing the patient’s percentage of REM sleep because the REM sleep is when OSA is most severe. Finally, ACE inhibitors may worsen OSA because of the adverse effects of cough and rhinopharyngeal inflammation, 2 effects that cease with discontinuation of the drug.
• Heart failure: OSA has not been established as a cause of heart failure, and whether OSA hastens death in patients with heart failure is uncertain. However, a 2007 study examined untreated OSA in patients with heart failure and reported that those with an apnea-hypopnea index (AHI) of greater than 15 had increased mortality compared with those with an AHI of less than 15.¹⁹ Also note that CPAP treatment in patients with OSA and heart failure may reduce mortality,²⁰ but the evidence is less than absolute because no randomized clinical trials have tested the effects.
• Arrhythmias: Patients with severe SDB have a 2- to 4-fold increased risk of experiencing nocturnal complex arrhythmia. Bradyarrhythmia is more common in OSA patients (occurs in approximately 10% of OSA patients), especially in the REM sleep state and when greater than 4% drop in oxygen saturation occurs. Additionally, atrioventricular block and asystole may occur in the absence of conduction disease. Also, premature ventricular contractions much more common in patients with OSA compared with those who do not have OSA (66% vs 0-12%, respectively), and they are most likely to occur during an apnea; however, CPAP treatment reduces the frequency of the premature ventricular contractions (by up to 58% reported in one study).
• Myocardial ischemia and infarction: OSA patients have double the prevalence of coronary artery disease, and an independent association has been shown between OSA and subclinical coronary artery disease, as demonstrated by coronary artery calcification. Further, OSA apparently affects the timing of sudden cardiac death because research shows that greater than 50% of sudden cardiac deaths that occur in OSA patients do so between 10 PM and 6 AM; the more common time for sudden cardiac death is from 6-11 AM. Men with untreated OSA and an AHI of greater than 30 had an increased number of fatal and nonfatal cardiovascular events, but treated OSA patients have a number of events similar to snorers who do not have OSA.

In a study of sleep-disordered breathing and nocturnal cardiac arrhythmias in older men, Mehra et al found that the likelihood of atrial fibrillation or complex ventricular ectopy increased along with the severity of sleep-disordered breathing. In addition, different forms of sleep-disordered breathing were associated with the different types of arrhythmias. Polysomnography in 2911 participants showed that the odds of atrial fibrillation (P = .01) and of complex ventricular ectopy (P <.001) increased with increasing quartiles of the respiratory disturbance index (a major index including all apneas and hypopneas).²¹
 
Central sleep apnea was more strongly associated with atrial fibrillation (odds ratio [OR], 2.69; 95% confidence interval [CI], 1.61-4.47) than with complex ventricular ectopy (OR, 1.27; 95% CI, 0.97-1.66). In contrast, obstructive sleep apnea and hypoxia was associated with complex ventricular ectopy; participants in the highest hypoxia category had an increased odds of complex ventricular ectopy (OR, 1.62; 95% CI, 1.23-2.14) compared with the lowest quartile. The results suggest that different sleep-related stresses may contribute to atrial and ventricular arrhythmogenesis in older men.²¹

Stroke

The Sleep Heart Health Study²² showed the strongest relationship was between OSA and stroke versus any other cardiovascular disease.

Patients with OSA are more likely to have a stroke and die than people without OSA. This correlation persists even if researchers control for the risk factors of age, sex, race, smoking, alcohol consumption, body mass index (BMI), diabetes mellitus, hyperlipidemia, atrial fibrillation, and hypertension. Time-to-event analyses have shown that patients with OSA (who were undergoing weight loss, CPAP, or surgery) have an increased hazard ratio for stroke or death of 1.97 (95% confidence interval, 1.12-3.48; P = .01). The risk of stroke or death was most severe in the quartile of patients with the most severe AHI. The hazard ratio increased to 3.30 (95% confidence interval, 1.74-6.26) when the AHI was greater than 36. This study was not powered sufficiently to determine if OSA treatment affects survival.

OSA is associated with an increased risk of type 2 diabetes. Whether OSA causes type 2 diabetes or whether it is associated with insulin resistance and diabetes is unclear. Use of CPAP can reverse insulin resistance. Sleep fragmentation, sleep deprivation, and hypoxemia (which all occur in OSA) are thought to play independent roles in glucose intolerance. Conflicting results show that reversal of glucose intolerance may occur when OSA is treated.

Race

African American individuals appear to be more predisposed to SDB than white persons. This increased predisposition varies according to age. The odds ratio is greater than 3 in children younger than 13 years and is 1.88 in persons younger than 25 years. In elderly African Americans, the risk is increased 2-fold.
 
Other populations that may be at increased risk include Mexican Americans and Pacific Islanders.

Sex

In adults, the male-to-female ratio is approximately 3:1. In population studies that have examined the incidence of OSA, women were less likely than men to have OSA and were less likely to be diagnosed early in the disease process. Survival rates are lower for women than for men, after an OSA diagnosis has been established by polysomnography, presumably due to the delayed OSA diagnosis.

Age

Aging is an important consideration of risk for OSA. OSA prevalence increases 2-3 times in older persons (>65 y) compared with individuals aged 30-64 years. After age 65 years, no further relative disparity is noted in the incidence of OSA. One explanation for this plateau is the relative increase in mortality in persons older than 65 years; however, data to support this contention, as attractive as it appears, are insufficient.  Scant data are available to help clinicians determine if the clinical management should differ between the age cohorts.

Clinical

History

• Snoring
• Sleepiness
• Spouse or significant other apnea report
• Hypertension
• Nonrestorative sleep (ie, "waking up as tired as when they went to bed")
• A choking sensation or gasping during the night; though in a very low proportion relative to the number of apneas they experience
• Morning headaches
• Patient report of "trouble sleeping"
• Insomnia
• Restless sleep
• Sore throat or dry mouth in the morning

Symptoms

• Cognitive deficits; memory and intellectual impairment
• Decreased vigilance
• Morning confusion
• Personality and mood changes, including depression and anxiety
• Sexual dysfunction, including impotence and decreased libido
• Gastroesophageal reflux

Risk factors

• Male sex
• Age 40-65 years
• Positive family history
• Body habitus
  • Overweight and obese
  • Central body fat distribution
  • Large neck girth (>17 in)
  • Increased Mallampati score (crowded-appearing pharyngeal airway)
  • UA abnormalities, including nasal congestion
  • Craniofacial abnormalities
• Menopause (in women)
• Alcohol use
• Sedative use
• Smoking
• Supine sleep position
• REM sleep state

Predictive value of clinical history and examination

• Predictive value
  • Disruptive snoring: A history of disruptive snoring has 71% sensitivity in predicting SDB.
  • Disruptive snoring and witnessed apneas: These factors taken together have 94% specificity for SDB.
• Questioning patients and others
  • Others: Obtaining a history from someone who has observed the patient's sleep behavior is important. Patients are usually unaware of snoring and/or sleepiness or may minimize these symptoms. Sleepiness may develop insidiously. Patients may be unaware that they are sleepy; that is, they may forget how normal alertness feels.
  • Patients: Question the patient about drowsiness in boring or monotonous situations and about sleepiness while driving.
• Sex-related differences
  • Reporting of symptoms: Women are twice as likely as men to not report snoring and apneas, even after one corrects for the RDI.
  • Presentation: Women commonly present with symptoms atypical of the classic presentation of OSA. Women are more likely than men to report fatigue and are less likely than men to report sleepiness.
  • Diagnosis and referrals: Although the male-to-female ratio for the prevalence of SDB in the general population is approximately 2-3:1, the male-to-female ratio for patients referred to sleep clinics for an evaluation of possible OSA is approximately 10:1. OSA appears to be notably underdiagnosed in females. A high index of suspicion must be maintained when screening females for SDB.
  • Menstruation: In 1 study, 43% of premenopausal women with SDB had menstrual irregularities that disappeared with the treatment of SDB.

Physical

• Obesity
  • Approximately 30% of patients with a BMI greater than 30 have OSA, and 50% of patients with a BMI greater than 40 have OSA.
  • In the United States, 20% of men and 25% of women have a BMI greater than 30.
  • Unfortunately, obesity has become an epidemic in industrialized nations. One study showed that the number of people with a BMI greater than 40 has tripled since 2000.²⁴
  • Patients with obesity hypoventilation syndrome and some patients with OSA may have evidence of pulmonary hypertension and right-sided heart failure.
• Large neck circumference
  • Neck circumference may correlate with OSA better than BMI.
  • In one study, subjects with OSA had a neck circumference 4 cm larger than subjects without OSA. In addition, neck circumference of 40 cm or greater had a sensitivity of 61% and a specificity of 93% for OSA, regardless of the person's sex.
• Abnormal Mallampati score (1-4 scale) 
• Systemic arterial hypertension present in approximately 50% of patients with OSA
• Congestive heart failure
• Pulmonary hypertension
• Stroke
• Metabolic syndrome
• Type 2 diabetes mellitus

Causes

• Structural factors
  • Structural factors related to craniofacial bony anatomy that predispose patients with OSA to pharyngeal collapse during sleep include the following:
    • Genetic variations (facial elongation, posterior facial compression)
    • Retrognathia and micrognathia
    • Mandibular hypoplasia
    • Brachycephalic head form
    • Inferior displacement of the hyoid
    • Pierre Robin syndrome
    • Down syndrome
    • Marfan syndrome
    • Prader-Willi syndrome
    • High, arched palate (particularly in women)
  • Structural factors related to nasal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include polyps, septal deviation, tumors, trauma, and stenosis.
  • Structural factors related to retropalatal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include (1) an elongated, posteriorly placed palate and uvula and (2) tonsil and adenoid hypertrophy (particularly in children).
  • Structural factors related to retroglossal obstruction that predispose patients with OSA to pharyngeal collapse during sleep include macroglossia and tumor.
• Nonstructural risk factors
  • Some nonstructural risk factors include obesity, age, male sex, postmenopausal state, and habitual snoring with daytime somnolence.
  • Familial factors also play a role. Families with a high incidence of OSA are reported. Relatives of patients with SDB have a 2- to 4-fold increased risk of SDB compared with control subjects.
  • Environmental exposures include smoke, environmental irritants or allergens, and alcohol and hypnotic-sedative medications.
  • Both hypothyroidism and acromegaly are associated with macroglossia and increased soft tissue mass in the pharyngeal region. They are associated with an increased risk of SDB. Hypothyroidism is also associated with myopathy that may contribute to UA dysfunction.

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