Sleep Apnea

 

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Definition/Description[edit | edit source]

Sleep apnea is a disorder in which breathing is interrupted or paused during sleep. The pauses in breathing can last a few seconds to minutes and are long enough to:
• disrupt sleep
• decrease level of oxygen in the blood
• increase level of carbon dioxide in the blood

These breathing interruptions can occur more than 30 times an hour and significantly impair the quality of sleep. Because of this, sleep apnea is a leading cause of excessive daytime sleepiness.

Prevalence[edit | edit source]

OSA appears to be more prevalent (2.5x increase) in the African-American population than the Caucasian population.[1] [2] On the other hand, OSA was more prevalent in American Indians, Hispanic adults, and Pacific Islanders when obesity played a large role.[2] Population-based studies have also shown that men have a 2-3x increased risk of developing OSA than women, and a women's risk of OSA increases during pregnancy.[1] [2] OSA can occur in childhood and adolescence, but is more common at middle-age (40-60 years old).[1] After the age of 65, the occurrence of OSA plateaus, and this may be due to an "increase in mortality rate from OSA or a remission of OSA with aging."[1](p1221) Genetics increase the likelihood of developing OSA and in the craniofacial morphology and its conditions that may contribute to OSA.[2]  Individuals with first-degree relatives who have OSA are 1.5-2 times more likely to have OSA.[2] OSA is also common in individuals who spend long periods of time sitting and driving, such as commercial trunk drivers.[3] 

Characteristics/Clinical Presentation[edit | edit source]

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Associated Co-morbidities[edit | edit source]

Individuals with Hypertension (HTN) have a higher incidence of OSA as well as the possibility of a causal relationship between HTN and OSA where treatment of OSA had lead to a decrease in HTN, specifically with middle-aged individuals.[4] Obesity is also commonly associated with OSA in which the excessive body weight affects the individual's breathing ability via increasing the amount of adipose around the airway structures, and the overall body.[1] [2] Those with congested heart failure (CHF), Type II Diabetes, pulmonary hypertension, and stroke have also been found to be at higher risk for OSA.[3] It has been noted that individuals with OSA had an increased risk of stroke, of nonfatal cardiovascular events, and of mortality from other causes, such as but not limited to, fatal cardiovascular events.[5] However, it was suggested that the OSA may be present before the onset of a stroke from studies showing individuals with OSA after other neurological deficits had recovered. [5]

Medications[edit | edit source]

Numerous studies have shown that the use of pharmacological interventions in the treatment and management of OSA have not been as effective as the use of PAP, specifically CPAP.[3] [6] [7] As discussed further below, CPAP is currently the gold standard in the treatment of OSA. 8 It has been shown that some drugs, such as Phentermine with extended release Topiramate (Qsymia), used for weight loss was able to decrease weight as well as AHI (Apnea Hypopnea Index).[6] However, more studies will have to be conducted to better correspond the use of these weight loss drugs and the improvement of OSA.

Drugs promoting wakefulness have also been studied as an adjunct therapy to help relieve the symptoms of daytime sleepiness of OSA.[6]Particularly, Modafinil had been studied with results of increased daily functioning, but if it were used by itself, individuals would eventually succumb to the long-term effects of OSA since Modafinil only treats the symptoms.[6] Recently in Europe, Modafinil was no longer available for those with OSA indications due to fear of abuse and lack of knowledge to the extent of its benefits.[6] Additionally, the long-term risks of cardiovascular effects from Modafinil are still unclear, so further research is required in its benefits versus cons.[7] 

Leukotriene Antagonists may be useful as adjunctive management.[7] A study noted a reduction in RDI (Respiratory Disturbance Index) and in adenoid size in children with OSA, but more research is required to substantiate its role as an intervention.[7] Donepezil has also been studied in treatment of OSA in Alzheimer's patients with the following positive outcomes: decrease AHI, improved REM sleep, and improved oxygen saturation.[7] Additionally, Mirtazapine was shown to decrease upper airway collapse, but may cause weight gain and sedation.[7] 

Inhaled corticosteroids have been shown to decrease AHI and nasal airway resistance, improving daytime wakefulness.[7] However, studies did not indicate improved breathing during sleep to normal, so it is not recommended as a treatment option at this time.[7] 

Finally, certain medications have been found to worsen OSA, and should not be prescribed to individuals with OSA. This includes CNS depressants (ex: opiates, benzodiazepines, barbiturates), certain Beta Blockers (ex: Propranolol), and some erectile dysfunction medications (ex: Sildenafil).[7] 

Diagnostic Tests/Lab Tests/Lab Values[edit | edit source]

Individuals suspected of OSA undergo a pretest assessment: a history, a clinical examination, and sleep questionnaires.[8]

  • History: possible risk factors, co-morbidities, snoring, and what a normal night of sleep is like to him/her.[9]
  • Clinical examination: nose, tonsils, palate, tongue, or upper airways.[9] Findings are predominantly inconclusive and requires training for proper assessment.[9]
  • Questionnaires: Epworth Sleepiness Score (ESS) for daytime sleepiness; Berlin questionnaire for common OSA risk factors and symptoms. [9]

For the diagnosis of sleep disorders, including OSA, the standard test is Level 1 polysomnography.[8] Individual is required to spend the night in a sleep laboratory, where a sleep technician is present, and 7 to 16+ channels are monitored.[8]These channels track the cardiovascular system, respiratory system, and neurologic system.[8] It can also monitor sleep duration, sleep arousals, and sleep stages.[8]

For those with a high probability of moderate to severe OSA, a good diagnostic test is Level 3 portable device (polygraph).[8] Portable monitors are brought into the individual’s home or preferred location.[8] These monitors look at at least 3 channels: oximetry, airflow, and respiratory effort in sleep.[8] It does not record sleep duration, arousals, sleep stages, or non respiratory sleep disorders.[8] Testing via these methods are most accurate when performed by an expert in sleep medicine.[9]

Etiology/Causes[edit | edit source]

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Systemic Involvement[edit | edit source]

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Medical Management (current best evidence)[edit | edit source]

Healthcare practitioners have utilized a variety of methods to treat individuals with OSA due to upper airway obstruction, including: weight reduction, sleep positioning, pharmacological treatments, oral appliances (OA), and upper air reconstructive or bypass surgeries.[3] Weight reduction via diet and exercise have shown to be beneficial, but it is not as effective when used by itself.[3] Positional maneuvers can be used to adjust sleeping position and avoid laying in supine with the help of positional devices, such as pillows.[3] The sleeping position can help increase airway size and opening.[3] Pharmacological interventions are not the ideal method for treatment of OSA, but topical nasal corticosteroids have been shown to be useful adjuncts to other OSA interventions.[3] 

Dental appliances that can be used for treatment are mandibular repositioning appliances (MRA) and tongue retaining devices (TRD).[3] MRA holds the mandible in an advanced position, and the TRD holds the tongue in a forward position, both in an attempt to avoid blockage of the upper airways while sleeping.[3] These oral appliances (OA) can be used for those with mild to moderate OSA, those who did not benefit from CPAP, and those who prefer OA.[3] Positive airway pressure (PAP) is the most common method of treatment for mild, moderate, and severe OSA.[3] PAP provides pneumatic splinting to maintain the opening of the upper airway and effectively decreases AHI (Apnea Hypopnea Index), which is the number of apnea or hypopnea episodes per hour of sleep.[3] [10] Normal AHI is less than 5 per hour.[10] PAP can be provided in several ways: continuous (CPAP, as the gold standard), (BPAP), and autotitrating (APAP) and via three interfaces: nasal, oral, or nasoral.[3] 

There are also surgical interventions to improve passages via nasal, oral, oropharyngeal, nasopharyngeal, hypopharyngeal, laryngeal, and global airways.[3] Surgeries are beneficial for those with severely obstructive anatomy and unsuccessful treatments with CPAPs or OAs.[3]These methods have shown varying degrees of success, so there is no consistent best treatment plan for all, but the combination of several of these therapies have proved to be effective.[3]

There is a new treatment option, the insertion of the Hypoglossal Nerve-Stimulating System (HGNS), that is currently being studied.[11] The Hypoglossal Nerve is the cranial nerve that innervates the tongue, especially the genioglossus muscle, and it plays a large role in maintaining airway patency.[11] Specifically, the genioglossus "protrudes the tongue, dilates the pharynx, and mitigates airflow obstruction during sleep."[11](p337)The study focused on HGNS via submental transcutaneous stimulation, direct fine wire stimulation, and direct hypoglossal stimulation.[11]Studies showed that submental transcutaneous stimulation aroused patients from sleep without clear improvements in the "airflow dynamics," but it is now being re-evaluated for the potential use of "prolonged, low-intensity transcutaneous stimulation" to increase lingual muscle tone and improve airway patency.[11](p338) In regards to the use of direct fine wire stimulation, it produced effective contractions of the genioglossus that improved pharyngeal patency as shown with and without simultaneous contractions of the lingual muslces.[11] Finally, the use of direct hypoglossal stimulation via implantation of "hypoglossal cuff electrodes" around the proximal and distal nerve trunk was able to increase pharyngeal patency and decrease pharyngeal collapsibility without arousing the patients.[11](p338) The implanted cuff electrodes had to be manually applied during sleep, but with the significant findings from the studies, there are currently "efforts to develop a fully implantable therapeutic HGNS system."[11](p338)

Physical Therapy Management (current best evidence)[edit | edit source]

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Differential Diagnosis[edit | edit source]

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Case Reports/ Case Studies[edit | edit source]

add links to case studies here (case studies should be added on new pages using the case study template)


1. Daoulah A, Ocheltree S, Al-Faifi S, Ahmed W, Asrar F, Lotfi A. Sleep apnea and severe bradyarrhythmia – an alternative treatment option: a case report. J Med Case Reports 2015; 9(1): 113-7.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4437673/

2. Voscopoulos C, Ladd D, Campana L, George E. Non-Invasive Respiratory Volume Monitoring to Detect Apnea in Post-Operative Patients: Case Series. J Clin Med Res 2014; 6(3): 209-214.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985564/

3. Guimarães T, Colen S, Cunali P, Rossi R, Dal-Fabbro C, Ferraz O, et al. Treatment of obstructive sleep apnea with mandibular advancement appliance over prostheses: A case report. Sleep Science 2015;8(2):103-106. 

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4608885/

4. Fang H, Miao N, Chen C, Sithole T, Chung M. Risk of Cancer in Patients with Insomnia, Parasomnia, and Obstructive Sleep Apnea: A Nationwide Nested Case-Control Study. J Cancer 2015;6(11):1140-1147.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4615350/

5. Cadby G, McArdle N, Briffa T, Hillman D, Simpson L, Knuiman M, et al. Severity of OSA Is an Independent Predictor of Incident Atrial Fibrillation Hospitalization in a Large Sleep-Clinic Cohort Chest. 2015;148(4):945-952.

http://www.sciencedirect.com/science/article/pii/S0012369215502833

Resources
[edit | edit source]

American Sleep Apnea Association

American Sleep Association (ASA)

Talk About Sleep

National Sleep Foundation

Recent Related Research (from Pubmed)[edit | edit source]

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References[edit | edit source]

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  1. ↑ 1.0 1.1 1.2 1.3 1.4 Young T, Peppard P, Gottlieb D. Epidemiology of Obstructive Sleep Apnea. Am J Respir Crit Care Med 2002;165(9):1217-1239. http://www.atsjournals.org/doi/full/10.1164/rccm.2109080#.Vu73OZMrKYU (accessed 20 March 2016).
  2. ↑ 2.0 2.1 2.2 2.3 2.4 2.5 Lam J, Sharma S, Lam B. Obstructive sleep apnoea: Definitions, epidemiology & natural history. Indian J Med Res 2010;131:165-170. http://pharexmedics.com/wp-content/uploads/2015/11/sleepapnea_ebook.pdf (accessed 3 April 2016).
  3. ↑ 3.00 3.01 3.02 3.03 3.04 3.05 3.06 3.07 3.08 3.09 3.10 3.11 3.12 3.13 3.14 3.15 3.16 Epstein L, Kristo D, Strollo Jr. P, Friedman N, Malhotra A, Patil S, et al. Clinical Guideline for the Evaluation, Management and Long-term Care of Obstructive Sleep Apnea in Adults. Journal of Clinical Sleep Medication 2009; 5(3): 263-276. http://pharexmedics.com/wp-content/uploads/2015/11/sleepapnea_ebook.pdf (accessed 3 April 2016).
  4. ↑ Nieto F, Young T, Lind B, Shahar E, Samet J, Redline S, et al. Association of Sleep-Disordered Breathing, Sleep Apnea, and Hypertension in a Large Community-Based Study. JAMA 2000; 283(14): 1829-1836. http://jama.jamanetwork.com/article.aspx?articleid=192578&resultclick=1 (accessed 20 March 2016).
  5. ↑ 5.0 5.1 Yaggi H, Concato J, Kernan W, Lichtman J, Brass L, Mohsenin V. Obstructive Sleep Apnea as a Risk Factor for Stroke and Death. The New England Journal of Medicine 2005; 353:2034-2041. http://www.nejm.org/doi/full/10.1056/NEJMoa043104#t=article (accessed 20 March 2016).
  6. ↑ 6.0 6.1 6.2 6.3 6.4 Booth A, Djavadkhani Y, Marshall N. A critical review of the treatment options available for obstructive sleep apnoea: an overview of the current literature available on treatment methods for obstructive sleep apnoea and future research directions. Bioscience Horizons 2014;7(0):1-8. http://biohorizons.oxfordjournals.org/content/7/hzu011.full.pdf (accessed 4 April 2016).
  7. ↑ 7.0 7.1 7.2 7.3 7.4 7.5 7.6 7.7 7.8 Tackett K, DeBellis H. USPharmacist.com. Pharmacotherapy Options in the Treatment of Obstructive Sleep Apnea. http://www.uspharmacist.com/content/d/feature/c/35564/ (accessed 5 April 5 2016).
  8. ↑ 8.0 8.1 8.2 8.3 8.4 8.5 8.6 8.7 8.8 10. Shayeb M, Topfer L, Stafinski T, Pawluk L, Menon D. Diagnostic accuracy of level 3 portable sleep tests versus level 1 polysomnography for sleep-disordered breathing: a systematic review and meta-analysis. Canadian Medical Association Journal 2013; 186(1):E25-E51. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3883848/pdf/18600e25.pdf (accessed 7 April 2016).
  9. ↑ 9.0 9.1 9.2 9.3 9.4 11. Maurer J. Early diagnosis of sleep related breathing disorders. GMS Current Topics in Otorhinolaryngology- Head and Neck Surgery 2010; 7(3): 1-20. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199834/ (accessed 7 April 2016).
  10. ↑ 10.0 10.1 Healthy Sleep Med Harvard Edu. Understanding the Results | Sleep Apnea. http://healthysleep.med.harvard.edu/sleep-apnea/diagnosing-osa/understanding-results (accessed 3 April 2016)
  11. ↑ 11.0 11.1 11.2 11.3 11.4 11.5 11.6 11.7 Schwartz A, Smith P, Oliven A. Electrical stimulation of the hypoglossal nerve: a potential therapy. Journal of Applied Physiology 2013;116(3):337-344. http://jap.physiology.org/content/116/3/337.full (accessed 3 April 2016).
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