Continuing Education Activity
Obstructive sleep-disordered breathing (SDB) is a syndrome of upper airway dysfunction during sleep that is characterized by snoring and/or increased respiratory effort secondary to greater upper airway resistance and pharyngeal collapsibility. Obstructive Sleep Apnea (OSA) is a sleep disorder that involves a significant decrease or cessation of airflow in the presence of breathing effort. An estimated 58% of moderate to severe obstructive sleep apnea is attributable to obesity. This activity illustrates the evaluation and treatment of obstructive sleep-disordered breathing and reviews the role of the interprofessional team in managing patients with this condition.
Objectives:
Review the etiology of Obstructive sleep-disordered breathing.
Describe the pathophysiology of Obstructive sleep-disordered breathing.
Summarize the treatment options for Obstructive sleep-disordered breathing.
Outline the use of collaboration and communication among the interprofessional team members to emphasize diet, weight loss, and use of CPAP, which will decrease morbidity and mortality in those with obstructive sleep-disordered breathing.
Access free multiple choice questions on this topic.
Introduction
Obstructive sleep-disordered breathing (SDB) is not a distinct disease, but rather a syndrome of upper airway dysfunction during sleep characterized by snoring and/or increased respiratory effort secondary to increased upper airway resistance and pharyngeal collapsibility. Obstructive Sleep Apnea (OSA), also referred to as obstructive sleep apnea-hypopnea, is a sleep disorder that involves cessation or a significant decrease in airflow in the presence of breathing effort.[1][2][3][4]
Hypopnea is defined as a recognizable, transient reduction, but not a complete cessation of, breathing for ten or more seconds.
The term “obstructive SDB” is used when symptoms of intermittent upper airway obstruction during sleep are present, but the severity of airway obstruction has not been defined by objective measures such as polysomnography.
The general characteristic of Obstructive Sleep Apnea is the increased collapsibility of the upper airway during sleep resulting in markedly reduced (hypopnea) or absent (apnea) airflow at the nose and/or mouth which is usually accompanied by oxyhemoglobin desaturation and is typically terminated by a brief micro-arousal.
Repeated episodes of apnea lead to a sustained reduction in oxyhemoglobin saturation and sleep fragmentation with diminished amounts of slow-wave and rapid eye movement (REM) sleep.
Etiology
The major predisposing factor for sleep apnea is excess body weight. It has been estimated that 58% of moderate to severe OSA is attributable to obesity. The etiology of OSA involves both structural and nonstructural factors, including genetic factors.[5][6][7][8]
Structural factors related to craniofacial bony anatomy that predisposes patients with OSA to pharyngeal collapse during sleep, e.g.:
Retrognathia and micrognathia
Maxillo-Mandibular hypoplasia
Adenotonsillar hypertrophy, particularly in children and young adults
High, arched palate (particularly in women)
Nonstructural risk factors for OSA include:
Smoking and alcohol consumption are often considered as risk factors for sleep apnea despite the limited evidence, especially in females.
It is well-known that alcohol consumption before going to bed worsens sleep apnea in males and that smoking is related to snoring in males and females.
Drinking more than 23 g of alcohol per day was related to oxygen desaturations and snoring in a study of Japanese females.
Epidemiology
Obstructive sleep apnoea (OSA) was considered a very rare disorder 30 years ago, but recent epidemiological studies show an astonishingly high prevalence. The prevalence of obstructive sleep apnoea syndrome (OSAS) ranged from 0.1% to 13%, but most studies demonstrated a frequency between 1% and 4%. Moderate to severe OSA has been found in up to 50% of men and 25% of women in the middle-aged population as defined by an apnea–hypopnea index (AHI) greater than or equal to 15. Over the past 30 years, obesity levels have risen dramatically, partly explaining the increase in OSA prevalence.
Pathophysiology
Muscle tone decrease throughout body during normal sleep and relaxation of upper airway dialtor muscles results in relative narrowing of air passage. The normal persons will not develop any significant symptoms due to this physiological phenomenon.
In patients with Sleep disorder the upper airway narrowing result in marked air flow turbulence with repetitive partial or complete obstruction of the pharynx during sleep. Despite increasing breathing efforts the upper airway collapse results in episodes of obstructive hypopneas or apneas affecting the sleep architecture.
Neuromuscular activity in the Upper Airway(UA), including reflex activity, decreases with sleep and this decrease may be more pronounced in patients with OSA. Reduced ventilatory motor output to upper airway muscles is believed to be the critical initiating event leading to UA obstruction; this effect is most pronounced in patients with a UA predisposed to collapse for anatomical reasons.
The Bernoulli effect plays an important dynamic role in OSA pathophysiology. By 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. Transmural pressure is the difference between intraluminal pressure and the surrounding tissue pressure.
This effect helps to partially explain why obese patients, particularly those with fat deposition in the neck, are most likely to have OSA.
OSA has been confirmed to be a causal factor in the pathogenesis of vascular dysfunction and hypertension.
History and Physical
Obstructive Sleep Apnea (OSA) symptoms begin insidiously and are often present for years before the patient is referred for evaluation.
Nocturnal symptoms may include:
Frequent loud snoring, witnessed apneas, restless sleep, nocturia and mouth breathing associated with the presence of obstructive SDB.
The hallmark of OSA are the witnessed apneas during sleep.
Daytime symptoms may include:
Nonrestorative sleep (e.g., “waking up as tired as when they went to bed”)
Morning headache, dry or a sore throat
Excessive daytime sleepiness (EDS) that usually begins during quiet activities
Daytime fatigue/tiredness
Cognitive deficits; memory and intellectual impairment
Sexual dysfunction, including impotence and decreased libido.
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.
Physical exam findings may include:
Obesity – Body mass index (BMI) greater than 30 kg/m
Large neck circumference – Greater than 43 cm (17 in) in men and 37 cm (15 in) in women
Abnormal (increased) Mallampati score (Mallampati score assessment (originally designed for quantifying different intubation) is a simple and fast method for assessing upper airway dimensions)
Enlarged, or "kissing," tonsils (3+ to 4+)
Retrognathia or micrognathia, macroglossia
Large degree of overjet
High-arched hard palate
Systemic arterial hypertension, present in approximately 50% of patients with OSA
Clinical assessment of tonsillar size (Brodsky score) is a weak predictor of presence or severity of obstructive SDB. During an evaluation, other differential diagnoses must be considered before labeling as sleep apnea.
Causes of nocturnal dyspnea include bronchial asthma, gastroesophageal reflux disease, and panic disorder. EDS might be a result of poor sleep hygiene, alcohol or drug abuse, atypical depression, and narcolepsy. Nocturia is prevalent and increases sharply with age. It might be caused by urological and other medical conditions such as hypertrophic benign prostate, diabetes mellitus, congestive heart failure, renal disease, diabetes insipidus and intake of diuretic medication.
Evaluation
The diagnostic management of OSA follows three steps: clinical interview, physical examination and sleep diagnostic tests.
According to the recommendations, physician assessment should include evaluation of risk factors and common presenting symptoms for obstructive sleep apnea (OSA). The best-documented risk factor is obesity.
Routine laboratory tests usually are not helpful in OSA in the absence of a specific indication. A thyrotropin test should be performed on any patient with possible OSA who has other signs or symptoms of hypothyroidism, particularly in elderly individuals.
Polysomnography is the gold standard for OSA diagnosis but is expensive and time-consuming.
Several questionnaires have been designed to identify patients at risk for OSA. The Berlin Questionnaire is a screening test that identifies 82.03% of the subjects as being at high risk of sleep apnea and 17.9% as being at low risk. In adults, an instrument derived from eight easily administered questions called the STOP-Bang questionnaire had been shown to stratify the risk of OSA, with a negative predictive value of 93% for moderate OSA and 96% for severe OSA. A comparison of five questionnaires – STOP, STOP-Bang, Berlin Questionnaire, Epworth Sleepiness Scale and four variable screening tool for stratifying risk of OSA show more sensitivity and less specificity for STOP-Bang (97.6 to 12.7%) and Berlin questionnaire (87 to 33%), and more specificity for the four variable screening tool (74.4%) and the Epworth Sleepiness Scale (67%).
Polysomnography (PSG): Involves simultaneous recording of physiologic variables during sleep like Electroencephalogram, Electro-oculogram, Chin electromyogram, electrocardiogram, respiratory effort, airflow, oxygenation, ventilation, snoring.
A PSG is necessary to diagnose OSA accurately and to assess treatment benefit. The duration of the diagnostic study should be at least six hours.
The following PSG findings are characteristic of OSA:
Apneic episodes occur in the presence of respiratory muscle effort.
Apneic episodes lasting 10 seconds or longer are considered clinically significant.
Patients may have a combination of apneas and hypopneas, or they may have one or the other exclusively.
Mixed apneas may occur.
The apnea-hypopnea index (AHI) is derived from the total number of apneas and hypopneas divided by the total sleep time.
Recommendations for cutoff levels on AHI include five-15 episodes per hour for mild, 15-30 episodes per hour for moderate, and more than 30 episodes per hour for severe.
Daytime sleepiness is also a main indication for the treatment of sleep apnea.
Treatment / Management
All patients with OSA should be counseled about the potential benefits of therapy and the hazards of going without treatment.[9][10][11][12]
Treatment consists of:
Non Pharmacological Measure including Diet, Devices and Surgery.
Pharmacological
Treatment depends in part on the severity of the sleep-disordered breathing (SDB). People with mild apnea have a wider variety of options, while people with moderate-to-severe apnea should be treated with nasal continuous positive airway pressure (CPAP).
CPAP treatment is indicated for all OSA patients with an RDI of 30 or more events per hour, regardless of symptoms, based on the increased risk of hypertension.
Treatment with CPAP is indicated for patients with an RDI of five to 30 events per hour for documented cardiovascular diseases to include hypertension, ischemic heart disease or stroke.
A randomized clinical trial shows significant improvement in all sleep-related symptoms, including snoring, witnessed apnoeas, choking, nightmares, daytime hypersomnolence (all p<0.001) and nocturia (p=0.049), in the CPAP group. In elderly patients with severe sleep apnea, CPAP treatment achieves an improvement in all domains of quality of life measured by QSQ, including day-time and night-time symptoms and social and emotional domains.
Effective CPAP is defined as the pressure level at which all apneas, hypopneas, respiratory-effort related arousals and snoring events are abolished. This pressure level could be maintained constantly throughout the night (Standard CPAP) or it could be automatically adjusted by the CPAP-device according to the patient needs (Auto-CPAP).
In patients with mild-to-severe obstructive sleep apnea who refuse or reject nasal CPAP therapy or who cannot tolerate CPAP due to persistent massive nasal mask air leakage or discomfort, BiPAP therapy should be tried next. If this therapy fails or is rejected, Oral Appliances should be considered.
Adequate adherence to PAP is defined as more than 4.5 hours of PAP use per night on a routine basis. Maximal improvement in neurocognitive symptoms can require as long as two months of PAP treatment.
Oral appliances are considered an alternative to CPAP for treating OSA. Mandibular advancement devices/tongue retaining devices reduce sleep-disordered breathing and subjective daytime sleepiness, improve the quality of life compared with control treatments and are recommended in the treatment of patients with mild to moderate OSA.[13]
General and behavioral measures, such as weight loss, avoidance of alcohol for four to six hours before bedtime, and sleeping on one’s side rather than on the stomach or back, are elements of conservative nonsurgical treatment.
Because obesity is a major predictive factor for OSA, weight reduction reduces the risk of OSA. The best data suggest that a 10% reduction in weight leads to a 26% reduction in the respiratory disturbance index (RDI).
Patients with sleep-disordered breathing should be advised to have a sufficient sleep and appropriate sleep hygiene.
Sleep hygiene instructions
Restricting caffeine after lunch
Restriction of other drinks or foods with activating properties (e.g. coke, tea, chocolate)
No alcohol intake in the evening
Restriction of smoking especially close to bedtime
Regular physical activity
Reduction of noises in the bedroom
Instructions to make the bed comfortable and to keep the bedroom dark during the night
Proper ventilation of the bedroom
Positional treatment aims at avoiding the supine horizontal posture while sleeping. This method might be effective in patients with positional OSA. Tennis ball attached to the back of a night-shirt, a variety of straps and vests with foam attachments, auditory alarms aimed at training patients to refrain from sleeping in the supine posture are a number of devices used for postural therapy.
Once diagnosed with OSA and started on nasal CPAP, patients require regular follow-up with a sleep specialist. Most patients are seen within two months of initiating CPAP to determine if it has been effective in alleviating symptoms (e.g., daytime sleepiness is substantially reduced or eliminated), to troubleshoot problems preventing the regular use of the CPAP and to reinforce the importance of daily use.
Surgery: Upper airway surgery and Barriatric Surgery for weight loss.
Medications
Dronabinol: Nonselective agonist of cannabinoids type I and type II receptor reduces central apneas and reduction in AHI index in small studies but still need further safety data to be estabilshed treatment.
Modafinil is approved by the US Food and Drug Administration (FDA) for use in patients who have residual daytime sleepiness despite optimal use of CPAP. The most improvement has been seen in patients who have taken modafinil at doses of 200-400 mg/d. The mechanism of action of modafinil in wakefulness is unknown. It has wake-promoting actions similar to sympathomimetic agents.
Armodafinil, the R-enantiomer of modafinil, is also now FDA approved for use in these patients.
Patients in whom noninvasive medical therapy (e.g., CPAP, BiPAP, OAS) fails should be offered surgical options.
Various surgical techniques are available for treatment of OSA. Their aim is to permanently increase upper airway patency and decrease pharyngeal resistance. Surgery may be applied as a first-line therapy in selected patients with mild OSA who have surgically correctible anatomical abnormalities contributing to upper airway collapse during sleep.
Nasal surgery, radiofrequency tonsil reduction, tongue base surgery, uvulopalatal flap, laser midline glossectomy, tongue suspension and genioglossus advancement cannot be recommended as single interventions. Uvulopalatopharyngoplasty, pillar implants, and hyoid suspension should only be considered in selected patients, and potential benefits should be weighed against the risk of long-term side-effects.
Hypoglossal nerve stimulation for the treatment of OSA may be a safe and effective alternative for improving OSA outcomes in individuals with moderate to severe OSA who have difficulties with CPAP therapy.
Pearls and Other Issues
The short-term prognosis, about symptoms such as daytime sleepiness and snoring, ranges from good to excellent with regular use of CPAP.
Severe OSA is a significant risk factor for the development of cardiovascular morbidity, which includes nonfatal myocardial infarction and stroke.
Patients with a history of ischemic stroke and sleep apnea who regularly used their CPAP device had a decreased mortality compared with those who did not use their CPAP device.
All patients should receive education about sleep and proper sleep hygiene, OSA and the risks of driving while sleepy. They also should receive education regarding the role of nasal CPAP and the importance of daily use, as well as training in the use of CPAP, from a physician, trained technician, or nurse for at least the first month of therapy. This training promotes long-term adherence with treatment.
Enhancing Healthcare Team Outcomes
The management of sleep apnea is with an interprofessional team because of the diverse symptoms and complex treatment. Patients with sleep apnea should be evaluated by a neurologist, cardiologist, bariatric surgeon, ENT surgeon, dietitian, pulmonologist and an oral surgeon. The treatment of these patients is initially non-pharmacological with emphasis on diet, weight loss and use of CPAP. The use of CPAP is associated with very low compliance rates and the next step is to recommend an oral appliance. The key is to educate the patient on lifestyle changes and reducing body weight. Until body weight is reduced, no treatment works consistently or reliably. At the same time, patients should be encouraged to reduce their risk of heart disease by discontinuing smoking, eating healthy and exercising. Unfortunately, patient compliance rates remain low and inadequately treated sleep apnea carries very high morbidity and mortality.[14][15] (Level V)
References
- 1.
Stöwhas AC, Lichtblau M, Bloch KE. [Obstructive Sleep Apnea Syndrome].
Praxis (Bern 1994). 2019 Jan;108(2):111-117. [
PubMed: 30722731]
- 2.
Leppänen T, Kulkas A, Mervaala E, Töyräs J. Increase in Body Mass Index Decreases Duration of Apneas and Hypopneas in Obstructive Sleep Apnea.
Respir Care. 2019 Jan;64(1):77-84. [
PubMed: 30578359]
- 3.
Ben Amar J, Ben Mansour A, Zaibi H, Ben Safta B, Dhahri B, Aouina H. Impact of smoking on the severity of Obstructive Sleep Apnea Hypopnea Syndrome.
Tunis Med. 2018 Aug-Sep;96(8-9):477-482. [
PubMed: 30430524]
- 4.
Szajerska-Kurasiewicz A, Lasyk D, Łoboda D, Simionescu K, Gibiński M, Pol-Romik J, Gołba KS. [How to avoid cardiovascular consequences of the obstructive sleep apnea syndrome?].
Wiad Lek. 2018;71(6):1254-1261. [
PubMed: 30267510]
- 5.
Awad MI, Kacker A. Nasal Obstruction Considerations in Sleep Apnea.
Otolaryngol Clin North Am. 2018 Oct;51(5):1003-1009. [
PubMed: 29934201]
- 6.
Lin J, Suurna M. Sleep Apnea and Sleep-Disordered Breathing.
Otolaryngol Clin North Am. 2018 Aug;51(4):827-833. [
PubMed: 29779616]
- 7.
Baratta F, Pastori D, Fabiani M, Fabiani V, Ceci F, Lillo R, Lolli V, Brunori M, Pannitteri G, Cravotto E, De Vito C, Angelico F, Del Ben M. Severity of OSAS, CPAP and cardiovascular events: A follow-up study.
Eur J Clin Invest. 2018 May;48(5):e12908. [
PubMed: 29424037]
- 8.
Muraki I, Wada H, Tanigawa T. Sleep apnea and type 2 diabetes.
J Diabetes Investig. 2018 Sep;9(5):991-997. [
PMC free article: PMC6123041] [
PubMed: 29453905]
- 9.
Scalzitti NJ, Sarber KM. Diagnosis and perioperative management in pediatric sleep-disordered breathing.
Paediatr Anaesth. 2018 Nov;28(11):940-946. [
PubMed: 30281185]
- 10.
Verburg FE, Bollen KHA, Donker HJ, Kramer GJC. The effectiveness of two types of MADS for OSA therapy.
Clin Oral Investig. 2018 Jun;22(5):1995-2003. [
PMC free article: PMC5945916] [
PubMed: 29214378]
- 11.
Ierardo G, Luzzi V, Polimeni A. [Obstructive Sleep Apnea Syndrome (OSAS): evaluation and treatment of odontostomatological problems].
Med Lav. 2017 Aug 28;108(4):293-296. [
PubMed: 28853428]
- 12.
Corso R, Russotto V, Gregoretti C, Cattano D. Perioperative management of obstructive sleep apnea: a systematic review.
Minerva Anestesiol. 2018 Jan;84(1):81-93. [
PubMed: 28402089]
- 13.
Dioguardi A, Al-Halawani M. Oral Appliances in Obstructive Sleep Apnea.
Otolaryngol Clin North Am. 2016 Dec;49(6):1343-1357. [
PubMed: 27720461]
- 14.
Gabric K, Matetic A, Vilovic M, Ticinovic Kurir T, Rusic D, Galic T, Jonjic I, Bozic J. Health-related quality of life in type 2 diabetes mellitus patients with different risk for obstructive sleep apnea.
Patient Prefer Adherence. 2018;12:765-773. [
PMC free article: PMC5953311] [
PubMed: 29785091]
- 15.
Karimi N, Kelava M, Kothari P, Zimmerman NM, Gillinov AM, Duncan AE. Patients at High Risk for Obstructive Sleep Apnea Are at Increased Risk for Atrial Fibrillation After Cardiac Surgery: A Cohort Analysis.
Anesth Analg. 2018 Jun;126(6):2025-2031. [
PubMed: 29533258]
Disclosure: Jawedulhadi Memon declares no relevant financial relationships with ineligible companies.
Disclosure: Susan Manganaro declares no relevant financial relationships with ineligible companies.
