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Obstructive Sleep Apnea Clinical Presentation

  • Author: Ralph Downey, III, PhD; Chief Editor: Zab Mosenifar, MD, FACP, FCCP  more...
 
Updated: Jun 03, 2016
 

History

Obstructive sleep apnea (OSA) symptoms generally begin insidiously and are often present for years before the patient is referred for evaluation.

Nocturnal symptoms may include the following:

  • Snoring, usually loud, habitual, and bothersome to others
  • Witnessed apneas, which often interrupt the snoring and end with a snort
  • Gasping and choking sensations that arouse the patient from sleep, though in a very low proportion relative to the number of apneas they experience
  • Nocturia
  • Insomnia
  • Restless sleep, with patients often experiencing frequent arousals and tossing or turning during the night

Daytime symptoms may include the following:

  • Nonrestorative sleep (ie, “waking up as tired as when they went to bed”)
  • Morning headache, dry or sore throat
  • Excessive daytime sleepiness (EDS) that usually begins during quiet activities (eg, reading, watching television); as the severity worsens, patients begin to feel sleepy during activities that generally require alertness (eg, school, work, driving).
  • Daytime fatigue/tiredness
  • Cognitive deficits; memory and intellectual impairment (short-term memory, concentration)
  • Decreased vigilance
  • Morning confusion
  • Personality and mood changes, including depression and anxiety
  • Sexual dysfunction, including impotence and decreased libido
  • Gastroesophageal reflux
  • Hypertension
  • Depression

EDS is one of the most common and difficult symptoms clinicians treat in patients with OSA. It is one of the most debilitating symptoms because it reduces quality of life, impairs daytime performance, and causes neurocognitive deficits (eg, memory deficits).

EDS is most frequently assessed by a sleep physician using the Epworth Sleepiness Scale (ESS). This questionnaire is used to help determine how frequently the patient is likely to doze off in 8 frequently encountered situations.

Although patients do not always accurately describe their sleepiness on this scale compared with objective measures, an ESS score greater than 10 is generally considered sleepy. However, a 2003 study showed that an ESS score of 12 is associated with a greater propensity to fall asleep on the Multiple Sleep Latency Test (MSLT), suggesting that 12 would be a better cutoff.[75]

The ESS score does not correlate well with the primary objective measurement of sleepiness, the MSLT,[76, 77] in that a higher ESS score does not mean shorter latencies on the MSLT. However, a higher ESS score does mean a greater likelihood of falling asleep on the MSLT.[75, 78] The ESS is useful for evaluating responses to treatment; the ESS score should decrease with effective treatment.

Although continuous positive airway pressure (CPAP) treatment quickly reverses EDS in most patients, not all patients use the CPAP device. Moreover, some patients remain sleepy despite effective CPAP treatment. In these patients, modafinil at 200-400 mg/d can effectively enhance alertness without changing CPAP use.[79] 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.

Most patients who do not report EDS do report being fatigued, having a lack of energy, or being tired during the day. In one study of 190 patients with OSA, patients were more likely to report lack of energy (62%), fatigue (57%), and tiredness (61%) than sleepiness (47%). When asked to choose their most significant symptom, 40% of patients chose lack of energy, compared with 22% for sleepiness.[80]

Partly because of their EDS, patients with OSA have substantially impaired daytime functioning, intellectual capacity, memory, psychomotor vigilance (decreased attention and concentration), and motor coordination. Causes include both sleep fragmentation and hypoxemia due to OSA. It is conceivable that these neurocognitive deficits could be reversed with CPAP. OSA patients showed an overrecruitment of brain regions compared with controls, in the presence of the same level of performance on a working-memory task.[81]

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Physical Examination

The general physical examination is frequently normal in patients with OSA, other than the presence of obesity, an enlarged neck circumference, and hypertension. Perform an evaluation of the upper airway in all patients, but particularly in nonobese adults with symptoms consistent with OSA.

Physical examination findings may include the following:

  • Obesity – Body mass index (BMI) greater than 30 kg/m 2
  • Large neck circumference – Greater than 43 cm (17 in) in men and 37 cm (15 in) in women
  • Abnormal (increased) Mallampati score
  • Narrowing of the lateral airway walls, which is an independent predictor of the presence of OSA in men but not women
  • Enlarged (ie, "kissing") tonsils (3+ to 4+) (see the image below)
  • Retrognathia or micrognathia
  • Large degree of overjet
  • High-arched hard palate
  • Systemic arterial hypertension, present in approximately 50% of patients with OSA
  • Congestive heart failure (CHF)
  • Pulmonary hypertension
  • Stroke
  • Metabolic syndrome
  • Type 2 diabetes mellitus
    Tonsil grades. Tonsil grades.

Approximately 30% of patients with a BMI greater than 30 and 50% of those 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.[82] Patients with obesity hypoventilation syndrome and some patients with OSA may have evidence of pulmonary hypertension and right-side heart failure.

A large neck circumference has been associated with an increased risk of OSA. 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.

The Mallampati score has been used for many years to identify patients at risk for difficult tracheal intubation. The classification provides a score of 1-4 based on the anatomic features of the airway seen when the patient opens his or her mouth and protrudes the tongue (see the image below). A 2006 study showed that for each 1-unit increase in the Mallampati score, the odds ratio of having OSA (defined by an apnea-hypopnea index [AHI] >5) increased by 2.5. In addition, the AHI increased by 5 events per hour.[83]

The Mallampati Classification is illustrated. The The Mallampati Classification is illustrated. The airway class is based on this visual heuristic.
In this polysomnogram summary graph, obstructive s In this polysomnogram summary graph, obstructive sleep apnea (OSA) severity and the degree of oxygen desaturation (SpO2%) worsen in rapid eye movement (REM) sleep (the black underlined sections) compared with non-REM sleep. This is often the case in OSA patients, especially in OSA patients with comorbid lung disease.
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Predictive Value of History and Physical Examination

The predictive value of initial clinical evaluation for OSA can be based on the following:

  • Disruptive snoring: A history of disruptive snoring has 71% sensitivity in predicting sleep-disordered breathing (SDB).
  • Disruptive snoring and witnessed apneas: These factors taken together have 94% specificity for SDB.

Questioning patients and others is necessary, as follows:

  • 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 include the following:

  • Reporting of symptoms: Women are twice as likely as men to not report snoring and apneas, even after one corrects for the respiratory disturbance index (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.

The mnemonic STOP is helpful and includes the following:

  • S: "Do you snore loudly, loud enough to be heard through a closed door?"
  • T: "Do you feel tired or fatigued during the daytime almost every day?"
  • O: "Has anyone observed that you stop breathing during sleep?"
  • P: "Do you have a history of high blood pressure with or without treatment?"

If the patient answers yes to more than 2 questions, the sensitivity of him or her having an AHI greater than 5 is 66% and the sensitivity of him or her having an AHI greater than 15 is 74%.

The mnemonic BANG is also useful, as follows:

  • B: BMI greater than 35
  • A: Age older than 50 years
  • N: Neck circumference greater than 43 cm (17 in)
  • G: Gender, male

If the criteria from both the STOP and BANG mnemonics are met, the sensitivity of the patient having an AHI of greater than 5 is 93% and an AHI of greater than 15 is 83%.[84]

Research has shown that the STOP-Bang questionnaire is both simple to use for busy clinicians and predictive of OSA. A 2012 study supports existing research indicating that screening in presurgical patients using the STOP-Bang score has a high probability of OSA detection.[85] Not all patient populations can be identified to the same degree of accuracy with the same tool, therefore research continues to find the best predictors for various patient populations.

Ramachandran et al have developed and validated a clinical score for predicting the diagnosis of OSA preoperatively in a general surgical population.[86] Their perioperative sleep apnea prediction (P-SAP) score is based on 3 demographic variables (age >43 y, male sex, and obesity), 3 history variables (history of snoring, diabetes mellitus type 2, and hypertension), and 3 airway measures (thick neck, modified Mallampati class 3 or 4, and reduced thyromental distance).

A diagnostic threshold P-SAP score of 2 or higher showed excellent sensitivity (0.939) but poor specificity (0.323), whereas a P-SAP score of 6 or higher had poor sensitivity (0.239) but excellent specificity (0.911).[86]

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Cardiovascular Disease in Obstructive Sleep Apnea

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.[87]

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.

A review by Somers et al yielded 2 particularly significant findings.[87] First, the data suggest that evaluation and treatment for OSA are not recommended in every patient with cardiac disease, but the threshold for a referral for polysomnography (PSG) and for treatment of OSA should be low. Second, 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.

Hypertension

Systemic hypertension is observed in 50-70% of patients with OSA. Several large cross-sectional studies have demonstrated that OSA is a risk factor for developing hypertension, independent of obesity, age, alcohol intake, and smoking.[39, 88]

More recently, subjects in the Wisconsin Cohort Study were prospectively monitored for the development of hypertension. The investigators found a dose-response relationship between the degree of OSA and the presence of hypertension 4 years later (odds ratio of 2.03 for an AHI of 5-15 and 2.89 for an AHI >15), independent of confounding variables.[89]

In the Sleep Heart Study,[90] 2470 subjects without OSA were followed for 5 years for the development of hypertension. In this cohort, the AHI was not an independent predictor of hypertension. Differences between the 2 study populations and differences in measurement of SDB events likely explain the discrepant results.

Treatment has been shown to decrease both systolic and diastolic hypertension. CPAP treatment has been shown to have moderate and variable effects on blood pressure (BP) in OSA patients.[91, 92, 93] However, no conclusive study has demonstrated that treating OSA with nasal CPAP lowers the blood pressure on a long-term basis.

CPAP has been investigated in nonsleepy hypertensive OSA patients. CPAP treatment for 1 year was associated with decreases in both systolic and diastolic BP. This effect was only evident in patients who used their CPAP device for more than 5.6 hours per night.[94]

Patients with hypertension and OSA may require CPAP and antihypertensive medication. A study examining the use of valsartan (160 mg/d) and CPAP in patients with newly diagnosed hypertension and newly diagnosed OSA found that together, the treatments synergistically reduced BP.[95] .Because OSA patients use CPAP regardless of whether they are taking medication for hypertension, the success of the CPAP-valsartan combination was the most important clinically relevant finding.

Decreased CPAP use was associated with higher nighttime systolic BP. Office BP, reported as entry criteria, was not reported after treatments in the results. Systolic and diastolic BP were not within normal limits on every time period measured.

Because of the reported negative correlations with CPAP use and nocturnal systolic BP as a function of the duration of CPAP use, an intervention to augment CPAP use would likely have been helpful to adequately assess CPAP’s effect on BP alone; the time spent on CPAP during this study was perhaps too low to demonstrate a larger change in BP parameters.

Although, as noted (see above), other studies suggest that the ability of CPAP to reduce hypertension require 5.6 hours of use per night, the subjects in this study used CPAP approximately 5 hours per night. Again, this limits the effect of CPAP on hypertension as a treatment alone and in combination with valsartan. On other hand, BP reductions with fewer hours of CPAP use than previous published studies further supports CPAP’s robust effect on BP and that fewer than 5.6 hours of CPAP use can lead to BP reductions.

Antihypertensive drug treatment does not improve OSA; however, clonidine, which is an REM sleep suppressant, may improve OSA indirectly by reducing the patient’s percentage of REM sleep because the REM sleep is when OSA is most severe. Finally, angiotensin-converting enzyme (ACE) inhibitor use may worsen OSA because of the adverse effects of cough and rhinopharyngeal inflammation, 2 effects that cease with discontinuation of the drug.

Atherosclerosis

OSA has been linked with the development of atherosclerosis. In a study of 36 subjects[96] with OSA and 16 matched controls, all without comorbidities, subjects with moderate-to-severe OSA were found to have increased carotid intima media thickness, increased pulse wave velocity, and increased carotid diameter, all of which are consistent with atherosclerosis. Abnormalities in these parameters were predicted by either the AHI or the degree of nocturnal desaturation. A 2007 follow-up study showed regression of these abnormalities after nasal CPAP.[97]

Congestive heart failure

OSA has not been established as a cause of heart failure, and whether it hastens death in patients with heart failure is uncertain. However, a 2007 study examining untreated OSA in patients with heart failure reported that those with an AHI higher than 15 had increased mortality compared with those with an AHI below 15.[98] CPAP treatment in patients with OSA and heart failure may reduce mortality,[99] but the evidence is less than absolute because no randomized clinical trials have tested the effects.

A study by Javaheri et al examined a study population of 30,719 patients with heart failure. Only 1,263 (4%) were suspected of having OSA.[100] After adjustments for age, sex, and comorbidities, patients with heart failure who were diagnosed with OSA and received treatment had a better 2-year survival rate than those who were not treated.

OSA patients with heart failure may be less likely to report daytime sleepiness, as measured by the Epworth Sleepiness Scale, compared to those OSA patients without HF. The authors of one study propose this is likely due to central adrenergic alerting mechanisms, as alertness is incompatible with sleep and may serve to mask subjective sleepiness.[101]

Cardiac 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 (occurring in approximately 10% of OSA patients), especially during REM sleep state and when a greater than 4% drop in oxygen saturation occurs. Additionally, atrioventricular block and asystole may occur in the absence of conduction disease.

Premature ventricular contractions (PVCs) also are much more common in patients who have OSA than in those who do not (66% vs 0-12%), and they are most likely to occur during an apnea; however, CPAP treatment reduces the frequency of the PVCs (by up to 58%, according to one study).

In a study of SDB and nocturnal cardiac arrhythmias in older men, Mehra et al found that the likelihood of atrial fibrillation (AF) or complex ventricular ectopy increased along with the severity of SDB. In addition, different forms of SDB were associated with the different types of arrhythmias. PSG in 2911 participants showed that the odds of AF and of complex ventricular ectopy increased with increasing quartiles of the RDI (a major index including all apneas and hypopneas).[102]

Myocardial ischemia and infarction

OSA patients have double the prevalence of coronary artery disease (CAD), and an independent association has been shown between OSA and subclinical CAD, as demonstrated by coronary artery calcification. Further, OSA apparently affects the timing of sudden cardiac death: research shows that more than 50% of the sudden cardiac deaths that occur in OSA patients do so between 10 PM and 6 AM, whereas 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.

Stroke

The Sleep Heart Health Study[103] showed that OSA had a stronger relationship with stroke than with any other cardiovascular disease.

Patients who have OSA are more likely to have a stroke and die than people who do not. This correlation persists even if researchers control for the risk factors of age, sex, race, smoking, alcohol consumption, BMI, diabetes mellitus, hyperlipidemia, AF, and hypertension.

Time-to-event analyses have shown that patients with OSA (who were undergoing weight loss, CPAP treatment, or surgery) have an increased hazard ratio for stroke or death of 1.97. 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 when the AHI was greater than 36. This study was not powered sufficiently to determine if obstructive sleep apnea treatment affects survival.

A number of prospective observational cohort studies have investigated the relationship between OSA and stroke. In the Wisconsin Cohort Study, an AHI of greater than 20 was associated with an increased risk of stroke over a 4-year follow-up (odds ratio, 4.31), although the odds ratio lost significance when corrected for age, BMI, and sex.[104]

In a study from Yale, after a mean follow-up of 3.4 years, an AHI of greater than 5 was associated with increased risk of stroke after adjustment for multiple confounders (hazard ratio, 1.97).[105]

In a group of elderly subjects followed over 6 years, patients with severe OSA (AHI >30/h) had an increased risk of stroke.[106] These studies provide evidence that OSA is a risk factor for the development of stroke.

Metabolic syndrome

OSA has an association with the metabolic syndrome. The metabolic syndrome is now recognized as an important contributor to the development of atherosclerosis and cardiovascular disease. As defined, a patient with the metabolic syndrome has increased fasting glucose levels, increased blood pressure, lipid abnormalities, and obesity. Evidence of proinflammatory and oxidative stress also exists in these patients. Growing evidence suggests that OSA may contribute to the metabolic derangements that characterize the metabolic syndrome (see the image below).

Potential relationship between obstructive sleep a Potential relationship between obstructive sleep apnea-hypopnea syndrome (OSAHS) and the metabolic syndrome. OSAHS has been associated with 3 of the 5 major clinical abnormalities associated with the metabolic syndrome, which is hypertension, insulin resistance, and proinflammatory/oxidative stress. OSAHS may be contributing to and/or modulating the severity of these metabolic abnormalities.

Multiple studies have shown that patients with OSA have increased glucose levels and increased insulin resistance.[107, 108, 109]

The most recent study, from 2004, was from the Sleep Heart Health Study.[109] In this study of 2000 research subjects, the prevalence of diabetic 2-hour glucose tolerance values rose from 9.3% in the group with an AHI less than 5-15% in the group with an AHI greater than 15. The odds ratio for having an abnormal glucose tolerance test result was 1.44 for the group with an AHI greater than 15; insulin resistance was also highest in this group.

Correlations were also noted for the degree of oxygen desaturation at night, indicating that the OSAHS may contribute to insulin resistance as a result of the hypoxemia that occurs with the syndrome. However, in the Wisconsin Cohort Study, subjects with OSAHS were no more likely to develop diabetes mellitus than subjects without OSAHS.[110]

OSA has been associated with increased production of reactive oxygen species[111] and other oxidative stress biomarkers.[112] It has also been associated with increased levels of several proinflammatory cytokines and markers associated with atherosclerosis. These include C-reactive protein (CRP) in both adults and adolescents,[113, 114] interleukin 6,[113] interleukin 18,[115] and matrix metalloproteinase 9.[116] However, at least one large epidemiologic study found no relationship between the severity of OSAHS and CRP levels.[117]

Oxidant-related microcirculatory endothelial dysfunction, in a group of patients who had no known vascular disease, improved when CPAP effectively treated the patient’s OSA, compared with no improvement in the control group.[118]

OSA has been associated with decreased production of nitric oxide.[119] Several studies have shown impaired vasodilator responses, as measured by either flow-mediated dilatation[120] or reactive hyperemic blood flow[121] techniques. Impaired flow-mediated dilatation was found to best correlate with the degree of oxygen desaturation in an epidemiologic cohort study.[122] Recent studies also indicate that cerebrovascular responses are impaired in patients with OSA.

Note that for most of these abnormalities associated with the metabolic syndrome, evidence from studies with a small number of subjects suggests that CPAP partially reverses the metabolic abnormality that is the focus of the study. That is, CPAP decreased insulin resistance, decreased lipid peroxidation, and increased vasodilator responses.

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Diabetes in Obstructive Sleep Apnea

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.

A 2009 study increases support for the role of OSA in exacerbating insulin control in patients with type 2 diabetes. This was found as an effect, independent of adiposity and other confounders.[123]

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Obstructive Sleep Apnea in Special Populations

Elderly persons

The prevalence of OSA increases with age.[36] However, the clinical significance of OSA in healthy, community-dwelling people has been questioned because these people do not show significant sequelae (eg, sleepiness).

Elderly patients presenting to sleep centers for evaluation have similar symptomatology (including EDS) and PSG results compared with patients who are not elderly, except that elderly patients underreport snoring as a chief complaint, they tend to be less obese, and they are less objectively sleepy based on MSLT results. Thus, all elderly people, particularly if overweight, should be questioned about snoring, witnessed apneas, and daytime sleepiness and should be referred for evaluation if necessary.

Age does not appear influence compliance with CPAP therapy.[124, 125] Thus, all elderly patients with significant and symptomatic OSAHS should be offered therapy.

Children

OSA has an estimated prevalence of 2% in children, affecting boys and girls in equal numbers. Children most often present with loud snoring and symptoms and signs of adenotonsillar hypertrophy. Adenotonsillar hypertrophy is the predisposing factor in the majority of cases, although obesity is becoming a more common factor as the prevalence of obesity in children increases. Craniofacial syndromes (eg, Pierre Robin syndrome) and trisomy 21 are also predisposing factors in children.

EDS is not a common symptom in children with OSA. Instead, school-aged children often report problems with schoolwork. Studies have shown improvement in cognitive function and/or grades after adenotonsillectomy in children with OSA.[126, 127, 128, 129] Evidence suggests an association between attention-deficit/hyperactivity disorder and OSA in children.[130, 131]

Also, study findings presented at the 2013 annual meeting of the American Thoracic Society suggest that childhood-onset asthma may raise the risk of subsequently developing OSA.[132] Asthma was an independent risk factor for incident OSA at 8 years. After sex, age, body mass index, nasal congestion or stuffiness, smoking status, and number of alcoholic drinks per week were controlled for, childhood-onset asthma was associated with a greater than 2-fold risk of developing OSA (odds ratio [OR], 2.16; P < .05), whereas adult-onset asthma increased the risk by more than half (OR, 1.57; P < .05).

Resection of the enlarged tonsils is the standard therapy for the majority of children presenting with OSA; CPAP use is becoming more common as more children with obesity and craniofacial syndromes are recognized to have OSA.

Pregnant women

Several case reports associate intrauterine growth restriction (also termed intrauterine growth retardation) in pregnant women with concomitant untreated OSA. A study from Sweden found that hypertension, preeclampsia, low Apgar scores, and intrauterine growth restriction were more common in habitually snoring pregnant women than in nonsnoring pregnant women.[133] Habitual snoring was independently predictive of hypertension and growth restriction after correcting for other factors (eg, weight, age, smoking status).

These data suggest a link between SDB (indicated by the snoring) and pregnancy complications. Therefore, evaluation of all pregnant women with signs and symptoms of OSA is recommended, and they should be started on CPAP to prevent complications.

One study, however, found that whereas self-reported snoring increased in pregnant women (23% of women by the last week of pregnancy in the Swedish study), the prevalence of OSA was not higher. This suggests that pregnant women should be referred for evaluation only if the snoring is loud, habitual, and associated with other symptoms of OSA.

Long-distance truck drivers

Older data indicated that commercial truck drivers have an increased prevalence of OSA. However, more recent data indicate that the prevalence is no different from the general population. Risk factors are similar to the general population but also include short sleep durations.

Evidence from both the United States and Australia found no relationship between OSA severity and crash rate in commercial drivers, except possibly for a relationship between severe OSA and severe crashes (those that involve multiple injuries or motor vehicle towed from the scene). However, because of the potential for risk, a review and guidelines have been published to guide the physician.[134, 135, 136]

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Contributor Information and Disclosures
Author

Ralph Downey, III, PhD Staff Sleep Specialist, Cleveland Clinic Foundation; Associate Clinical Professor of Medicine, Loma Linda University School of Medicine

Ralph Downey, III, PhD is a member of the following medical societies: American Academy of Sleep Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

James A Rowley, MD Professor, Fellowship Program Director, Department of Medicine, Division of Pulmonary, Critical Care and Sleep Medicine, Wayne State University School of Medicine

James A Rowley, MD is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Himanshu Wickramasinghe, MD, MBBS Attending Physician, Pulmonary, Critical Care, and Sleep Medicine, Henry Mayo Newhall Memorial Hospital

Himanshu Wickramasinghe, MD, MBBS is a member of the following medical societies: American College of Chest Physicians, American Thoracic Society

Disclosure: Nothing to disclose.

Philip M Gold, MD Professor of Medicine, Chief of Pulmonary and Critical Care Medicine, Medical Director of Respiratory Care, Loma Linda University Medical Center

Philip M Gold, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Heart Association, American Lung Association, American Medical Association, American Thoracic Society, California Medical Association, Society of Critical Care Medicine, Undersea and Hyperbaric Medical Society, California Thoracic Society, American Federation for Clinical Research, Association of Subspecialty Professors

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Daniel R Ouellette, MD, FCCP Associate Professor of Medicine, Wayne State University School of Medicine; Chair of the Clinical Competency Committee, Pulmonary and Critical Care Fellowship Program, Senior Staff and Attending Physician, Division of Pulmonary and Critical Care Medicine, Henry Ford Health System; Chair, Guideline Oversight Committee, American College of Chest Physicians

Daniel R Ouellette, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, Society of Critical Care Medicine, American Thoracic Society

Disclosure: Nothing to disclose.

Chief Editor

Zab Mosenifar, MD, FACP, FCCP Geri and Richard Brawerman Chair in Pulmonary and Critical Care Medicine, Professor and Executive Vice Chairman, Department of Medicine, Medical Director, Women's Guild Lung Institute, Cedars Sinai Medical Center, University of California, Los Angeles, David Geffen School of Medicine

Zab Mosenifar, MD, FACP, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Federation for Medical Research, American Thoracic Society

Disclosure: Nothing to disclose.

Additional Contributors

Sat Sharma, MD, FRCPC Professor and Head, Division of Pulmonary Medicine, Department of Internal Medicine, University of Manitoba; Site Director, Respiratory Medicine, St Boniface General Hospital

Sat Sharma, MD, FRCPC is a member of the following medical societies: American Academy of Sleep Medicine, American College of Chest Physicians, American College of Physicians-American Society of Internal Medicine, American Thoracic Society, Canadian Medical Association, Royal College of Physicians and Surgeons of Canada, Royal Society of Medicine, Society of Critical Care Medicine, World Medical Association

Disclosure: Nothing to disclose.

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Sleep-related disordered breathing continuum ranging from simple snoring to obstructive sleep apnea (OSA). Upper airway resistance syndrome (UARS) occupies an intermediate position between these extremes. Note areas of overlap among the conditions.
In this polysomnogram summary graph, obstructive sleep apnea (OSA) severity and the degree of oxygen desaturation (SpO2%) worsen in rapid eye movement (REM) sleep (the black underlined sections) compared with non-REM sleep. This is often the case in OSA patients, especially in OSA patients with comorbid lung disease.
MRI rendering of a patient without obstructive sleep apnea (OSA) (left panel) and a patient with OSA (right panel).
Top image is 3-dimensional surface renderings of the upper airway demonstrating the effect of progressive increases in continuous positive airway pressure (CPAP) from 0-15 cm of water on upper-airway volume in a patient with upper airway narrowing. CPAP significantly increases airway volume in the retropalatal (RP) and retroglossal (RG) regions. Bottom image is soft tissue images in the same patient in the RP region at analogous levels of CPAP. With increasing CPAP, the upper airway progressively enlarges, particularly in the lateral dimension. Note the progressive thinning of the lateral pharyngeal walls as the level of CPAP increases. Little movement occurs in the parapharyngeal fat pads, the white structures lateral to the airway. The first image in each series depicts the baseline upper airway narrowing present in this patient.
Potential relationship between obstructive sleep apnea-hypopnea syndrome (OSAHS) and the metabolic syndrome. OSAHS has been associated with 3 of the 5 major clinical abnormalities associated with the metabolic syndrome, which is hypertension, insulin resistance, and proinflammatory/oxidative stress. OSAHS may be contributing to and/or modulating the severity of these metabolic abnormalities.
The Mallampati Classification is illustrated. The airway class is based on this visual heuristic.
Tonsil grades.
Obstructive sleep apnea. Note the absence of flow (red arrow) despite paradoxical respiratory effort (green arrow).
Central sleep apnea (thick areas). Note the absence of both flow and respiratory effort (green double arrows).
Comparison of a central apnea (box) and obstructive apnea (circle).
Mixed sleep apnea. Note that the apnea (orange arrow) begins as a central apnea (effort absent; red double arrow) and ends as an obstructive apnea (effort present; green double arrow). Note the arousal (blue arrow) that terminates the apnea and the desaturation (purple arrow) that follows.
A 2-minute recording of sleep showing 4 hypopneas (thick arrows) and associated oxygen desaturations (red arrows). This recording illustrates the recurrent nature of the sleep-disordered breathing observed in many patients.
Effect of nasal continuous positive airway pressure (CPAP) on oxygen saturation in sleep apnea. The upper portion of this figure shows the raw oxygen saturation trace from 1 night of a sleep study. Below the raw trace are vertical lines that indicate the presence of either an apnea or hypopnea. Before CPAP, frequent respiratory events with significant desaturations occurred. During the night, CPAP was applied, resulting in the elimination of the apnea and hypopneas and normalization of the oxygen trace.
Examples of good (upper panel) and poor (lower panel) compliance. In the upper panel, the patient is using continuous positive airway pressure (CPAP) most nights and generally for more than 4 hours (solid black line). In the lower panel, the patient is using CPAP infrequently and, when used, is wearing the CPAP device for less than 4 hours.
Approach to a patient with excessive daytime sleepiness after treatment with nasal continuous positive airway pressure.
 
 
 
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