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 Table of Contents  
CASE REPORT
Year : 2021  |  Volume : 9  |  Issue : 1  |  Page : 127-131

Oropharyngeal muscle strengthening exercises in obstructive sleep apnea


Department of Physiotherapy, School of Allied Medical Sciences, Lovely Professional University, Phagwara, Punjab, India

Date of Submission08-Dec-2020
Date of Decision26-Jan-2021
Date of Acceptance27-Jan-2021
Date of Web Publication26-Jun-2021

Correspondence Address:
Dr. Anujot Kaur
Department of Physiotherapy, School of Allied Medical Sciences, Lovely Professional University, Phagwara, Punjab
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/amhs.amhs_318_20

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  Abstract 


Obstructive sleep apnea (OSA) is a common pattern of sleep-disordered breathing in the adult population. It is characterized by episodes of partial or complete cessation of breathing during sleep due to the collapse of the pharyngeal airway. OSA is involved in the pathogenesis of numerous cardiovascular and metabolic disorders. This study brings forth the case of a 54-year-old male who was experiencing breathing difficulty during sleep with recent episodes of sudden loss of consciousness followed by labored breathing and excessive sweating. He was diagnosed and treated for a bifascicular block. This was followed by the additional diagnosis of OSA. The treatment plan comprised a set of Oropharyngeal Muscle-Strengthening Exercises (OMSE). The daytime sleepiness was quantified using the Epworth Sleepiness Scale (ESS). Over the span of 6 weeks, an improvement of −2 points on the score was documented, which is considered to be statistically significant according to the ESS scale. From this case report, the authors concluded that OMSE can be used as an alternative treatment option for mild OSA. OMSE is a noninvasive, cost-effective intervention for mild OSA that provides long-term benefits to the patient. Timely diagnosis and intervention can help in improving the quality of life of the patient.

Keywords: Cardiovascular disease, obstructive sleep apnea, oropharyngeal exercises, polysomnography, sleep-disordered breathing


How to cite this article:
Chawla NS, Kaur A, Subramanian T. Oropharyngeal muscle strengthening exercises in obstructive sleep apnea. Arch Med Health Sci 2021;9:127-31

How to cite this URL:
Chawla NS, Kaur A, Subramanian T. Oropharyngeal muscle strengthening exercises in obstructive sleep apnea. Arch Med Health Sci [serial online] 2021 [cited 2021 Aug 1];9:127-31. Available from: https://www.amhsjournal.org/text.asp?2021/9/1/127/319394




  Introduction Top


The abnormal collapse of the oropharyngeal airway during sleep leading to episodes of cessation of breathing and the resulting repetitive arousals is termed as obstructive sleep apnea (OSA).[1] This leads to periodic falls in the oxygen saturation levels and severe sleep fragmentation. There could be various causes of OSA and the common symptoms include snoring, headache upon waking up, increased daytime sleepiness, and mild impairments in the cognitive performance.[2] The prevalence of OSA is 13% among the population of North India.[3]

Certainly, there are various risk factors that classify a set of population to be more at risk for developing OSA. It is more prevalent in the male population of age above 45 years. Obesity, regular smoking, alcohol consumption, inherent craniofacial malformations, positive family history of OSA, and comorbid respiratory pathologies are other risk factors for OSA.[3],[4] In OSA, breathing ceases partially or completely from a few seconds to minutes followed by the awakening of the patient. The repeated arousals tend to be the cause of daytime sleepiness and increased fatigability of the patient.[5] Untreated OSA is also known to be associated with various cardiovascular morbidities and metabolic disorders like diabetes mellitus (DM) type-2.[5],[6]

The diagnosis of OSA can be established by taking a detailed history of the patient accounting for the risk factors and analyzing the anthropometric measurements of the patient such as body mass index, neck circumference, and craniovertebral angle.[3] To confirm the diagnosis, a polysomnographic study is considered as the gold standard measure.[7] Home-based sleep apnea testing is another option. It is based on the analysis of the respiratory events and the changes in oxyhemoglobin saturation.[7] Questionnaires such as Epworth Sleepiness Scale (ESS) are also reliable screening tools for quantifying the daytime sleepiness in OSA.[8]

There are various treatment approaches to OSA. Of all those, continuous positive airway pressure (CPAP) is considered as highly effective treatment.[5] However, according to the evidence reported, the adherence of the OSA patients to CPAP therapy is low.[9] Positional therapy, a variety of oral appliances, surgical procedures, and weight control strategies are some other known treatment options for OSA.[5]

Oropharyngeal muscle strengthening via exercises and electrical stimulation are novel strategies in OSA management. The pathology behind OSA could by multifactorial. Different anatomical and physiological factors could be listed as possible culprits behind this. The upper airway dilator muscles play a vital role in maintaining the patency of the upper airway. The basic principle behind oropharyngeal muscle strengthening for OSA is the increase in the tone of the upper airway musculature which prevents the collapse of the pharyngeal airway. Thus, it would help in decreasing the apneic episodes and relieving the symptoms of OSA.[10]


  Case Report Top


The patient, a 54-year-old male, a businessman by profession, a known case of DM type 2 and hypertension for 13 years, well managed on medications. The anthropometric measurements are mentioned in [Table 1]. He has made certain dietary modifications as advised by the physician and follows an exercise regime of 30 min/day, almost regularly. He has maintained the weight of 82–84 kg (180–185 lbs) for the past 5–8 years. The patient has a history of occasional alcohol consumption, once in few months. He is otherwise a nonsmoker and has no other addictions. He also denies any sorts of occupational exposures to excessive pollution.
Table 1: Anthropometric measurements

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He also has a history of hyperlipidemia. He is on medications for the same and yet his lipid profile shows elevated triglycerides. There is no other relevant medical history reported by the patient. His wife reported about his nighttime snoring for 10 years. He had been previously evaluated for the same and diagnosed to have a deviated nasal septum. No intervention was given for the same. He also has a history of chronic nasal congestion and uses a nasal decongestant spray for more than 20 years.

His wife also reported his lately increased fatigability and daytime sleepiness. Upon being questioned about his sleep routine, the patient mentioned that he usually gets 6–7 h of sleep every day but still feels tired throughout the day. He does not usually get any naps during the day. He drinks three cups of tea per day for many years now. Recently, he presented to the physician with the chief complaints of 3–4 episodes of fainting, falling onto the ground unconscious, and waking up from sleep at midnight with breathlessness and excessive sweating. He was admitted and evaluated for the same at a hospital in Gurgaon.

The patient got an electrocardiography (ECG) [Figure 1] and coronary angiography for evaluation of his symptoms. The findings are summarized in [Table 3]. The ECG findings were consistent with bifascicular block. The coronary angiography revealed normal coronaries. Thus, he underwent a pacemaker implantation and was discharged the next day in stable condition. However, the sleep issues still continued to happen.
Table 3: Physiotherapy assessment for obstructive sleep apnea

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Figure 1: Electrocardiography tracings of patient immediately after an episode of loss of consciousness

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His wife is a light sleeper. She reported that there would be a sudden break in his snoring, followed by cessation of breathing for a short period of time. She would nudge him and rub his feet to wake him up and he would be breathless and sweaty. Thus, the patient underwent a portable home-based sleep study for further evaluation. Based on this sleep study, the Apnea–Hypopnea Index value came out to be 7.2. This is consistent with the diagnosis of mild sleep apnea. The summary of the initial investigations have been mentioned in [Table 2].
Table 2: Preliminary investigations and findings for cardiac and sleep issues

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The patient was referred to a physical therapist (PT) for respiratory physiotherapy. A written consent form was obtained from the patient. A summary of PT evaluation is mentioned in [Table 4]. The ESS of the patient on day 0 was 11. This is consistent with mild excessive daytime sleepiness. The PT decided to put the patient on oropharyngeal muscle strengthening exercise (OMSE) protocol described in [Table 4]. The exercises were demonstrated to the patient and then supervised sessions once a day and home protocol once in the evening were prescribed for a period of 6 weeks and then a follow-up was done after 3 months. A significant improvement was seen in the ESS [Table 4].
Table 4: Oropharyngeal muscle-strengthening exercise regimen

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  Discussion Top


Diagnosing a patient with OSA, clinically, is a bit of a riddle. Since the patient did not present with the conventional chief complaints, it was imperative that the primary diagnosis of OSA was missed. More emphasis was given to the cardiac symptoms and preliminary investigations were centered on them. This case report brings forth the process of arriving at the diagnosis of OSA. We also highlight the physiotherapy perspective on the treatment of OSA.

OSA is characterized by the episodic cessation of breathing due to the collapse of the pharyngeal airway while the patient is asleep. This leads to repetitive partial or complete arousals of the patient from sleep. It is considered to be a potentially life-threatening condition. Over the past few decades, extensive research work has been carried out to establish the association of OSA with cardiovascular diseases.[11] Sleep deprivation resulting from OSA leads to increased sympathetic activity and pro-inflammatory responses. These phenomena are thought to be responsible behind the pathogenesis of the cardiovascular sequelae of OSA.[12]

OSA is often underdiagnosed. Certain risk factors have been identified such as hypertension, obesity, craniofacial abnormalities, and alcohol consumption.[4],[13] Patients with untreated OSA are thus at a greater risk of cardiovascular morbidities such as hypertension, arrhythmias, congestive cardiac failure, and strokes.[13] Sleep deprivation in turn causes hypertension and obesity attributable to increased serum cortisol levels.[14] Therefore, OSA triggers a vicious cycle of these events.

The recent episodes of fainting and falling to the ground followed by excessive sweating brought the patient to the local general practitioner. The cessation of breathing during his sleep was also reported by the wife. Initial ECG showed first-degree atrioventricular conduction block with left axis deviation. The reports were suggestive of right bundle branch block and left anterior fascicular block. According to the statistics, almost 50% of OSA patients eventually develop arrhythmias.[15] For further management, the patient was referred to a multispecialty hospital in Gurgaon. Pacemaker implantation was done to correct the bifascicular block. The surgery was uncomplicated and the patient was discharged the next day.

Since the sleep issues continued to happen, the patient underwent a home-based sleep study. Once the diagnosis of OSA was established, various treatment options were explained to the patient. Following a patient-centric clinical decision-making process, the patient was put on the OMSE regime.[16] The rationale behind the use of OMSE for sleep apnea is that strengthening would increase the upper airway dilator muscle tone. This increase in muscle tone helps in maintaining the patency of the pharyngeal airway.[16] This in turn prevents the collapse of the airway by counteracting the negative transmural pressure, thus reducing the number of apneas/hypopneas during sleep.[16]

For maintaining the patency of the pharyngeal airway during normal respiration, the muscles of the upper airway and thoracic respiratory muscles work in co-ordination with each other. The activation and contraction of the muscles such as the omohyoid, sternohyoid, genioglossus, and digastric helps to prevent the collapse of the lumen of the pharyngeal airway. These are termed as upper airway dilator muscles. In case of OSA, a set of articulatory and non-articulatory exercises are used to strengthen these dilator muscles.[17] OMSE have been known to be effective in reducing the neck circumference. These exercises also aim at tongue repositioning and mandibular elevation to counteract the tendency of the upper airway to collapse.[18]

Thus, the goal of OMSE regime that the patient was put on was to restore the normal breathing pattern of the patient during sleep and to provide a cost-effective, non-invasive solution to the patient. ESS was used as an outcome measure for quantifying the improvement in the daytime sleepiness resulting from OSA. ESS was administered once before the intervention, after 6 weeks, and then upon the 3-month follow-up.[19] The scores were documented and suggested statistically significant improvement.

As this case demonstrates, the OMSE program can be successfully used in patients with mild OSA. This treatment option shows optimal results and can prevent the detrimental sequelae of OSA. The results offer long-term benefits to the patients.[17] The limitation of the study is the use of less reliable outcome measures. Only ESS has been used which is a patient-reported outcome measure. Standardized outcome measures such as oropharyngeal electromyogram study and oximetry could be used in further studies to present more concrete support of this intervention.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

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Pinto AM, Devaraj U, Ramachandran P, Joseph B, D'Souza GA. Obstructive sleep Apnea in a rural population in South India: Feasibility of health care workers to administer level III sleep study. Lung India 2018;35:301-6.  Back to cited text no. 1
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Maspero C, Giannini L, Galbiati G, Rosso G, Farronato G. Obstructive sleep apnea syndrome: A literature review. Minerva Stomatol 2015;64:97-109.  Back to cited text no. 2
    
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Sharma SK, Kumpawat S, Banga A, Goel A. Prevalence and risk factors of obstructive sleep apnea syndrome in a population of Delhi, India. Chest 2006;130:149-56.  Back to cited text no. 3
    
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Stierer T, Punjabi NM. Demographics and diagnosis of obstructive sleep apnea. Anesthesiol Clin North Am 2005;23:405-20.  Back to cited text no. 4
    
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Spicuzza L, Caruso D, Di Maria G. Obstructive sleep apnoea syndrome and its management. Ther Adv Chronic Dis 2015;6:273-85.  Back to cited text no. 5
    
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Nannapaneni S, Ramar K, Surani S. Effect of obstructive sleep apnea on Type 2 diabetes mellitus: A comprehensive literature review. World J Diabetes 2013;4:238-44.  Back to cited text no. 6
    
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Laratta CR, Ayas NT, Povitz M, Pendharkar SR. Diagnosis and treatment of obstructive sleep apnea in adults. CMAJ 2017;189:E1481-8.  Back to cited text no. 7
    
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Spira AP, Beaudreau SA, Stone KL, Kezirian EJ, Lui LY, Redline S, et al. Reliability and validity of the Pittsburgh sleep quality index and the Epworth sleepiness scale in older men. J Gerontol A Biol Sci Med Sci 2012;67:433-9.  Back to cited text no. 8
    
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Rotenberg BW, Murariu D, Pang KP. Trends in CPAP adherence over twenty years of data collection: A flattened curve. J Otolaryngol Head Neck Surg 2016;45:43.  Back to cited text no. 9
    
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Guimarães KC, Drager LF, Genta PR, Marcondes BF, Lorenzi-Filho G. Effects of oropharyngeal exercises on patients with moderate obstructive sleep apnea syndrome. Am J Respir Crit Care Med 2009;179:962-6.  Back to cited text no. 10
    
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Jean-Louis G, Zizi F, Clark LT, Brown CD, McFarlane SI. Obstructive sleep apnea and cardiovascular disease: Role of the metabolic syndrome and its components. J Clin Sleep Med 2008;4:261-72.  Back to cited text no. 11
    
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Medic G, Wille M, Hemels ME. Short-and long-term health consequences of sleep disruption. Nat Sci Sleep 2017;9:151-61.  Back to cited text no. 12
    
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Gonzaga C, Bertolami A, Bertolami M, Amodeo C, Calhoun D. Obstructive sleep apnea, hypertension and cardiovascular diseases. J Hum Hypertension 2015;29:705-12.  Back to cited text no. 13
    
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Hanson JA, Huecker MR. Sleep Deprivation. Treasure Island, FL: StatPearls Publishing; 2020.  Back to cited text no. 14
    
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Shankar S, Gupta SS, Rojas-Marte G, Demir S, Saxena A, Obiagwu C, et al. Electrocardiographic associations seen with obstructive sleep apnea. Sleep Disord 2019;2019:9704785.  Back to cited text no. 15
    
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Mohamed AS, Sharshar RS, Elkolaly RM, Serageldin SM. Upper airway muscle exercises outcome in patients with obstructive sleep apnea syndrome. Egypt J Chest Dis Tuberculosis 2017;66:121-5.  Back to cited text no. 16
    
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Younis A, Baz H, Abd El Maksoud A. Upper Airway Exercises in Patients With Obstructive Sleep Apnea. Egypt J Chest Dis Tuberculosis: Mansoura University; 2010.  Back to cited text no. 17
    
18.
Chiu KL, Ryan CM, Shiota S, ET AL. Fluid shift by lower body positive pressure increases pharyngeal resistence in healthy subjects. Am J Respir Crit Care Med 2006;174:1378-83.  Back to cited text no. 18
    
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Ye D, Chen C, Song D, Shen M, Liu H, Zhang S, et al. Oropharyngeal muscle exercise therapy improves signs and symptoms of post-stroke moderate obstructive sleep apnea syndrome. Front Neurol 2018;9:912.  Back to cited text no. 19
    


    Figures

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    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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