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 Table of Contents  
REVIEW ARTICLE
Year : 2019  |  Volume : 4  |  Issue : 1  |  Page : 9-13

Obstructive sleep apnea: 2019 update


Department of Medicine, Intensive Care Unit, Northside Hospital Forsyth, Cumming, Georgia, USA

Date of Web Publication1-Oct-2019

Correspondence Address:
Dr. Anthony P Kimani
Intensive Care Unit, Northside Hospital Forsyth, Cumming, Georgia
USA
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/njct.njct_9_19

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  Abstract 


Obstructive sleep apnea (OSA) is a common and potentially life-threatening breathing disorder that remains significantly under-diagnosed worldwide. This review summarizes recent epidemiological research that sheds light on OSA in the African context for the first time, and describes the pathophysiology, clinical manifestations and treatment options. The author is hopeful that this information will assist clinicians in diagnosing and managing OSA patients, and inspire researchers to develop better diagnostic and treatment modalities.

Keywords: Clinical diagnosis, clinical manifestations, epidemiology in Africa, medical and surgical management, obstructive sleep apnea, pathophysiology


How to cite this article:
Kimani AP. Obstructive sleep apnea: 2019 update. Niger J Cardiovasc Thorac Surg 2019;4:9-13

How to cite this URL:
Kimani AP. Obstructive sleep apnea: 2019 update. Niger J Cardiovasc Thorac Surg [serial online] 2019 [cited 2019 Dec 12];4:9-13. Available from: http://www.nigjourcvtsurg.org/text.asp?2019/4/1/9/268469




  Introduction Top


There are few diseases with as many variations in clinical manifestations and multi-system impact as obstructive sleep apnea (OSA). Often perceived as an amusing condition associated with loud snoring and excessive sleepiness, OSA can be a life-threatening ailment associated with severe cardiovascular, neurological and respiratory derangements. This article is written to raise the awareness of clinicians on the African continent.


  Epidemiology of Obstructive Sleep Apnea Top


There is an ongoing unprecedented global epidemic of obesity resulting from radical changes in lifestyle. In addition, advances in medicine and public health have reversed the morbidity and mortality of many infectious diseases, resulting in longer human life expectancies. This crisis transcends age, gender, political, cultural, and socioeconomic lines and is resulting in tremendous increases in obesity-related illness such as high blood pressure, diabetes, heart disease, and obstructive sleep apnea (OSA). OSA is a breathing disorder caused by upper airway collapse due to failure of the normal compensatory mechanisms that preserve patency during sleep. In sleep, there is a recurrent interruption of breathing and snoring caused by periodic obstruction of airflow at the level of the upper airway during inhalation. This causes chronic sleep deprivation that manifests as excessive somnolence, reduced mental ability, driving and work-related accidents and lower overall work productivity. The health consequences of moderate and severe OSA can be serious or even life-threatening. OSA has been associated with hypertension, diabetes, heart failure, stroke, and treatment-resistant depression, even when obesity is factored out.

Children under the age of 8 years usually have OSA on the basis of adenoid and tonsillar hypertrophy or chronic nasal obstruction. Increasingly though, OSA is being diagnosed in adolescents where it tends to persist into adulthood, particularly if they are obese and male.[1] OSA becomes more prevalent with aging and also occurs in the nonobese. African–Americans and Asians are at greater risk, but all the reasons for this have not been identified. However, it is estimated that 80% of people with OSA remain undiagnosed and untreated due to a general lack of awareness of this major health problem, and the small number of trained physicians in the young science of sleep medicine.

The global epidemiology of OSA was studied by the International Research Group and published in the Lancet Respiratory Medicine in August 2019.[2] The startling discovery was that globally about 936 million people have OSA, with moderate or severe disease afflicting 425 million of them. This was an almost ten-fold increase from the 2007 World Health Organization estimate of 100 million people. These statistics do not include individuals under the age of 30 or over 69 years and do not address gender differences. There were no data available from any African country, and hence, the number of affected individuals was estimated based on the characteristics of similar racial groups in other nations. The study reported the top 10 affected countries by the population size [Table 1]. The global prevalence of OSA ranged from 8% (Hong Kong and Macao) to 77% (Brunei and Malaysia), with the prevalence of moderate-or-severe OSA also varying widely. In Africa, the lowest estimated OSA prevalence is in the central and eastern regions, with the north and west being most affected. Nations with significant OSA in the age group of 30–69 years were Algeria (54%), Angola, Benin, Côte d'Ivoire, Gambia, Togo, and Nigeria (60%), and Mali with the highest in Africa (65%). In high-OSA regions, there are stark differences between neighboring nations that bear further investigation.
Table 1: Top ten countries worldwide by obstructive sleep apnea population size

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  Pathophysiology Top


Upper airway abnormalities associated with OSA include an abnormally small airway cross-sectional area that subjects the pharynx to collapse; an enlarged tongue that can obstruct the airway by moving posteriorly into the airway space during sleep; a recessed lower jaw that can increase tissue pressure surrounding the airway and subject it to collapse; an enlarged soft palate that can impinge on airway space when breathing; or compromised pharyngeal dilator muscles that fail to keep the airway open when inhaling, causing momentary obstruction of airflow. Some patients also have high loop gain and low arousal thresholds that perpetuate cycles of upper airway collapse [Figure 1].
Figure 1: Mechanisms of upper airway obstruction.

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There are several theoretical pathophysiological mechanisms for OSA-related morbidity and mortality. Hypoxia may contribute to stress-related catecholamine and cortisol release during sleep, with the sympathetic hyperactivity contributing to daytime hypertension and metabolic dysregulation. Repetitive cycles of this process may lead or contribute to stroke, myocardial infarction, congestive heart failure, or sudden death. Episodic hypoxia may accelerate the atherosclerotic process by activating vascular inflammatory pathways. Cardiac dysrhythmias and reduction in cardiac output as a result of swings in intrathoracic pressure may also result from OSA. Data suggest that platelet activation may occur from several of these mechanisms, further compromising vascular integrity and raising the risk of arterial and venous thrombosis.


  Clinical Manifestations Top


The classic symptoms of loud snoring punctuated by periods of prolonged breathing cessation during sleep are usually reported by a concerned bed partner or family member but are often underplayed by the patient. Many patients, when carefully questioned, experience clusters of other symptoms such as debilitating sleepiness or insomnia, recurrent dreams involving drowning or suffocation, gastroesophageal reflux, morning headaches, dry mouth, nocturia, low libido, and difficulty controlling blood pressure, depression, or blood sugar despite compliance with medications. Children may paradoxically present with hyperactivity. A recent clinical vignette in the New England Journal of Medicine [3] is illustrative of the evaluation process in adults.


  Diagnosis Top


Formal diagnosis involves recording sleep stages and cardiorespiratory status with either a portable monitoring unit or by the gold standard of polysomnography in a sleep center. An average overnight apnea–hypopnea index (AHI) of more than five combined apneas (breath-hold over 10 s) and hypopneas (shallow respiratory efforts accompanied either by >3% oxygen desaturation or arousal) per hour qualifies as OSA. Mild OSA is defined as AHI between 6 and 14, moderate is AHI 15–29, and severe OSA is an AHI over 29. Severe AHI is associated with premature mortality from cardiovascular disease and stroke. The degree of oxygen desaturation during sleep is not used as a measure of severity, but this author is of the opinion that it should.


  Treatment Modalities Top


Medical devices

  1. Positive airway pressure (PAP) – The current state of the art in treating mild-to-severe OSA involves the use of mechanical systems that pump air (sometimes enriched with oxygen) into the upper airway through a mask that fits tightly over the nose and/or mouth as depicted in [Figure 2]. This pressurized jet of air called continuous PAP (CPAP), or bilevel positive airway pressure (inspiratory and a lower expiratory PAP) counteracts upper airway collapse by providing a “pneumatic splint.” This technology is effective but has the disadvantages of being expensive to purchase and maintain and uncomfortable and impractical to use. Typical problems that reduce compliance with PAP include claustrophobia, problems with mask fit causing leaks and skin and eye irritation, nasal congestion, and oral dryness. Unfortunately, PAP is poorly accepted by many patients. Usually, only those with the worst symptoms continue treatment for a prolonged period. The overall long-term compliance with CPAP is relatively low. The high clinical efficacy but low patient compliance reduces clinical effectiveness. It has been difficult to determine therefore whether the modest impact of CPAP on important cardiovascular risks such as hypertension and diabetes are a function of low effect size resulting from noncompliance or indicate that reduction of the airways' obstruction does not have substantial beneficial effects on the other coexisting risk factors
  2. Mandibular advancement devices (MADs) – MAD is custom-fabricated dental prostheses that treat mild-to-moderate OSA by applying traction to advance the mandible, thereby limiting posterior tongue movement associated with upper airway obstruction during sleep [Figure 3]. MAD generally have high initial acceptance among patients. However, with their lower clinical efficacy and limited treatment range, disease alleviation using MAD is compromised. Noncustom “boil and bite” oral appliances marketed for snoring are not effective in treating OSA
  3. Nasal expiratory valves – These are one-way valves formed into a Band-Aid that blocks the nostrils so that the user cannot exhale through the nose [Figure 4]. This creates a back pressure that keeps the upper airway open. These devices treat mild OSA at best and are recommended as the third-line treatment after CPAP and MAD.
Figure 2: Positive airway pressure.

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Figure 3: Mandibular advancement device.

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Figure 4: Nasal expiratory pressure valves.

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Surgical approaches

  1. Bariatric surgery – OSA in super-obese patients can be reversed by major weight loss, but this rarely happens without bariatric (gastric banding, stapling, or bypass) surgery. Weight loss surgery is usually curative. Gastric banding is illustrated in [Figure 5]
  2. Uvulopalatopharyngoplasty (UPPP) – This surgery involves removing the sagging tissues of the soft palate with or without partial glossectomy, i.e., and carving away the back of the tongue to create room for airflow [Figure 6]. This procedure is of dubious clinical benefit and may only work in the mildest forms of OSA. It can lead to swallowing impediments
  3. Soft-palate implants – Surgeons insert struts 18 mm in length and 1.5 mm in diameter into the soft palate to keep it from caving in and blocking the upper airway [Figure 7]. The subsequent healing of tissue around the implants stiffens the soft palate, thereby reducing the relaxation and vibration of the tissue. As is the case for UPPP, this treatment is of limited value in treating most OSA patients
  4. Hypoglossal nerve stimulation – This newer approach for refractory severe OSA involves implanting a generator that electrically stimulates the tongue to keep it in front of the mouth during sleep. It is not suitable for some people with the complete collapse of the soft palate. [Figure 8] shows the anatomical location of the leads, whereas [Figure 9] identifies the device on a portable anterior–posterior chest radiograph in a human with previous median sternotomy and a right central venous catheter.
Figure 5: Bariatric surgery: Gastric banding.

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Figure 6: Oral cavity after uvulopalatopharyngoplasty.

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Figure 7: Soft-palate implants.

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Figure 8: Hypoglossal nerve stimulation.

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Figure 9: Chest radiograph appearance of implanted hypoglossal nerve stimulator.

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CPAP has been the dominant treatment modality for moderate-to-severe OSA for over 30 years. CPAP-treated patients compared with a no-treatment control group repeatedly demonstrate a statistically significant improvement in daytime sleepiness, quality of life, and cognitive function. Clinical research has clearly demonstrated that OSA is a modifiable risk factor that significantly increases the probability of major cardiovascular and cerebrovascular events independent of confounding comorbid risk factors. However, there are no convincing data from prospective randomized controlled studies demonstrating that CPAP treatment results in cardiovascular or cerebrovascular risk reduction. There are observational data that suggest a role for CPAP in the secondary prevention of recurrent stroke and cardiovascular disease in patients with OSA.


  Conclusion Top


There is a desperate need for effective, affordable, and user-friendly OSA therapy to serve people in both developed and emerging nations. The recent Lancet study's ten-fold revision of the global burden of OSA is bound to reinvigorate research and entrepreneurial activity in the OSA diagnosis, treatment, and monitoring industry. Hopefully, these treatments will be available in the next few years to the millions of undiagnosed patients who suffer and die from this preventable disease. In the interim, I expect to see a wave of mobile device-based applications (apps) that evolve to medical-grade OSA self-diagnostic systems in much the same way cardiac monitoring has progressed. This will raise the awareness of OSA and lead more people to treatment.

Financial support and sponsorship

Nil.

Conflicts of interest

Dr. Kimani holds patents in obstructive sleep apnea diagnosis, treatment, and monitoring. He is a co-founder and Chief Medical Officer of Dreamscape Medical, an obstructive sleep apnea technology development company based in the USA.



 
  References Top

1.
Veasey SC, Rosen IM. Obstructive sleep apnea in adults. N Engl J Med 2019;380:1442-9.  Back to cited text no. 1
    
2.
Benjafield AV, Ayas NT, Eastwood PR, Heinzer R, Mary I, Morrell MJ, et al. Estimation of the global prevalence and burden of obstructive sleep apnea: A literature based analysis. Lancet Respir Med 2019;7:687-98.  Back to cited text no. 2
    
3.
Chan KC, Au CT, Hui LL, Ng SK, Wing YK, Li AM, et al. How OSA evolves from childhood to young adulthood: Natural history from a 10-year follow-up study. Chest 2019;156:120-30.  Back to cited text no. 3
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9]
 
 
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