Obstructive Sleep Apnea

Our eighth episode is sure to keep you awake and learning while helping your patients sleep. Come learn about obstructive sleep apnea!!

Show Notes

Intro:

Hey everyone and welcome to The Oto Approach, a podcast created by medical students for medical students, to teach you about all things otolaryngology. I'm your host Aileen, and today we're going to talk about obstructive sleep apnea. Tag along for a discussion about this common otolaryngology presentation. 

There are three main kinds of sleep apnea: obstructive sleep apnea, central sleep apnea, and mixed sleep apnea [1]. Obstructive sleep apnea, otherwise known as OSA, will be the focus of this episode, as it is the most common of the three types and is amenable to referral and treatment by an otolaryngologist [1]. OSA occurs most commonly when the muscles in the throat and neck relax causing the soft tissues to collapse on the upper airway during sleep, resulting in obstructions to breathing, hence its name [1]. Central sleep apnea is the result of the brain temporarily failing to send the necessary signals to the muscles involved in breathing [1]. Mixed sleep apnea is the combination of obstructive and central sleep apnea [1]. 

OSA is a common condition. In fact, recent Canadian data shows the self-reported prevalence of diagnosed OSA is 6.4%, and nearly 30% of Canadians are at intermediate or high risk for OSA [2].

Patients with OSA experience pauses in breathing (known as apneas) or decreases in breathing (known as (hi pop neas) hypopneas) due to muscle relaxation and excess soft tissue in the upper airway leading to collapse and obstruction during sleep [3,4]. More specifically, apneas are defined as a decrease of >/= 90% in respiratory airflow for 10 seconds or longer [5]. Hypopneas are defined as a >/=30% decrease in respiratory airflow for 10 seconds or longer with a >/= 4% decrease in oxygen saturation [5]. Complete airway obstruction will cause an  (app knee ick) apneic episode, whereas partial obstruction will cause a (hi pop knee ick) hypopneic episode [6]. These episodes stimulate breathing efforts against the obstructed airway, causing the patient to wake up and reopen their airway - this awakening is termed arousal [3,7]. The awakening can be accompanied by a gasp, but it is so brief that the patient often doesn’t remember it [1], but it may be observed by their bed partner or anyone observing them sleeping. 

Frequent arousals cause poor sleep quality resulting in decreased daytime attention, alertness, and memory, and increased risk for mood disorders, cardiovascular and respiratory diseases, endocrine dysfunction, and mortality [8]. Pediatric patients with OSA can also experience failure to thrive, behavioural difficulties, and sleep disturbances such as night terrors and enuresis (en ur e sis) or bed-wetting [9].

Patho-physiology:

Let’s dive a bit deeper into the pathophysiology of OSA.

As mentioned, OSA occurs when the soft tissues of the upper airway collapse and cause obstruction to breathing. Patients with OSA can maintain patency of their airway during waking hours, and will maintain bursts of patency throughout the night [3]. However, the decreased neuromuscular tone accompanied with deep sleep can result in relaxation of the muscles that maintain the upper airway, resulting in airway obstruction, and subsequent arousal of the patient to “catch their breath” [3]. The three major areas of obstruction are the nose, the palate, and the hypopharynx.  Many muscles are involved in maintaining patency of the upper airway including the extrinsic muscles of the tongue, the hyoid bone muscle group (suprahyoid muscles), the pharyngeal constrictors, and the muscles of the soft palate [10]. Two muscles that have been studied and thought to play a key role in the pathophysiology of OSA are the (gene ea glossus) genioglossus and the tensor palatini (pala teenie) [10]. Airway collapse can happen at any of the three parts of the pharynx, which is subdivided into the nasopharynx, oropharynx, and hypopharynx. However, the oropharynx is the most common location [11]. 

In addition, factors that put patients at increased risk for OSA include anatomically narrow airways or comorbidities that impede breathing and/or cause extrinsic compression of the airway, such as obesity [1,3,4].

The pathophysiology of obstructive sleep apnea in children often involves a combination of upper airway structural and neuromuscular abnormalities [12]. The structural abnormality that contributes most frequently in children is enlarged adenoids and palatine tonsils (adenotonsillar hypertrophy) [9,12]. These may be large relative to the size of a child’s oropharynx and can be the major contributing factor to their OSA [9,12]. Finally, syndromes that affect children's craniofacial anatomy can also contribute to OSA [9,12].

Presentation/history:

Now let’s talk about how a patient with sleep apnea would typically present in the clinic. Sleep apnea has different presentations in the adult and pediatric populations.

Adults will often complain of excessive daytime fatigue, poor concentration, or morning headaches [13]. The patient or their partners may have noticed loud snoring, gasping for air, choking on their breath, or pauses in their breathing as they sleep, called witnessed apneic spells [13]. 

A thorough history and physical examination can be used to gather additional proof of suspected OSA. There are a variety of clinical tools used to clarify an OSA diagnosis. The Epworth sleepiness scale can be used to quantify daytime sleepiness, and is therefore useful in assessing sleep disordered breathing, including OSA, and many other conditions [14]. Patients are provided with a list of situations, and the patient is asked to use the scale to rate the likelihood that they would doze off or fall asleep during those situations [14]. Another one that is commonly used is the STOP-BANG questionnaire [15]. STOP-BANG is a mnemonic to guide our clinical examination and can be used to qualify the likelihood of OSA. The S stands for snoring, T for daytime tiredness, O for observed apneic/hypopneic episodes, P for high blood pressure, B for body mass index above 35 m/kg^2, A for age above 50, N for neck circumference greater than 40 cm, and finally G for male gender [15].

Once you have gone through the STOP-BANG criteria add up all their positive screens. A STOP-BANG score of 0-2 is considered low risk for OSA, 3-4 is intermediate, and 5-8 is high risk [15]. Patients who screen positive for 2 out of 4 of the STOP questions and are male, have a BMI >35 kg/m2, or neck circumference >40cm are also considered high risk for OSA [15]. 

For any patient presenting with sleep concerns, it is important to take a detailed sleep history. Clarify their sleep position (supine, lateral decubitus, head of bed elevation). Characterize the patient’s sleep concern, such as daytime sleeping, amount of sleep per night, bed and wake-up times, and the regularity of their sleep schedule [16]. We also want to inquire about their sleep hygiene, such as their meal schedule particularly before bed, screen time before bed, and exercise frequency and timing [16]. Also consider social factors which may impact their sleep, this includes alcohol, smoking or vaping (be sure to ask about both tobacco and marijuanna), recreational drug use and its relation to their sleep, stimulant use including caffeine, life stressors, and their work - particularly for shift workers [16]. Finally, a past medical history should be taken including asking about current medication use (including over the counter medications and supplements), psychiatric illnesses or symptoms, and other health conditions, this can shed light on contributing factors and if they are experiencing health complications associated with OSA [16].

Beyond those mentioned in the STOP-BANG criteria, other features to look for on physical examination include RETRO NATHIA retrognathia, which describes the mandible being positioned posteriorly compared to maxilla. One should also assess for a short neck length which is measured from chin to thyroid cartilage. To assess the oropharynx, inspect the patient's mouth with a flashlight or headlight and look for oropharyngeal crowding [17-19]. Various methods have been described to quantify oropharynx crowding. Two commonly used methods are the Mallampati and the Friedman scoring systems which rank oropharynx crowding based on 4 classes. These two scoring systems use the same criteria as one another [17,19-21]. While the Mallampati scoring system is assessed with the patient’s tongue protruded beyond their teeth (out of their mouth), the Friedman classification is done with the tongue inside the mouth [19,20]. Class 1 describes visibility of the soft palate, uvula, and tonsillar pillars [19-21]. Class 2 is when only the soft palate and uvula can be visualized [19-21]. Class 3 is when only the soft palate and base of uvula are visualized [19-21]. And the most severe - class 4 is when only the hard palate can be visualized [19-21]. The nose should be examined with anterior rhinoscopy by students. The otolaryngologist is also going to use an endoscope to examine the sinonasal cavity, base of tongue, hypopharynx, and larynx.

Pediatric patients tend to present differently than adults. Often, parents will note that the child snores loud enough to hear through the walls and this occurs regularly (>/= 3x/week). They may also witness a pause in the child’s breathing (observed apneic spell) [9]. Additionally, the child may experience excessive sleepiness throughout the day and require unplanned naps [9,22]. Disruptions in sleep are common as well - this includes wetting the bed, otherwise known as enuresis, night terrors or nightmares where children wake up in the night and will often disrupt their bedsheets, and/or frequent waking through the night [9,22]. The most important piece of social history to ask about in the pediatric population for OSA presentations is second-hand smoke exposure. It is also important to ask about recurrent otitis media, tonsillitis or pharyngitis as the predisposing factors for these presentations overlap greatly with those for OSA.

During the pediatric physical examination, start with inspection for craniofacial abnormalities, which may predispose patients to narrow airways and OSA, the body habitus of the child, and any signs of poor growth[22,23]. Next, it is important to listen and observe the child speak and breathe. Don’t tell them you are doing this as they may change their natural behavior! Does their voice sound hyponasal? Are they consistent mouth breathers? Hyponasal speech and consistent mouth breathing suggest enlarged adenoids. Adenotonsillar hypertrophy is a common pediatric otolaryngology presentation, and is clinically important when evaluating OSA. Usually, the tonsils and adenoids continue to increase in size after birth, and growth of these structures peaks around 2-4 years of age [12]. Another growth spurt of these structures may occur during puberty [12]. While often there is hypertrophy of both the adenoids and tonsils together, it is possible for either adenoids or the tonsils to cause OSA in isolation.

Lastly, look inside the patient's mouth with a light source, you can also use a tongue depressor for better visualization of the oropharynx, but be aware that many pediatric patients may not enjoy this too much and may become less cooperative. Because of this, you should save the oral examination for the end of your history and physical. You can also ask the patient to say “aaaahhhh” to elevate their soft palate and allow for better visualization of the oropharynx/tonsils. Start by describing the tonsils qualitatively - are they erythematous? Is there any exudate? (this is relevant to infectious or inflammatory presentations but not really part of the examination for OSA). Do you identify any differences between the palatine tonsils?  It is also important to describe any asymmetry in the size of the tonsils. This can be especially relevant in adult patients because asymmetric tonsils can be the first sign of tonsillar cancer [24]. Then proceed to describe their size. Tonsil size is typically graded on a scale of 0-4+. Zero means the tonsils are not visible, indicating that they are within the tonsillar fossa, or that the patient had a previous tonsillectomy [23]. One+ means the tonsils occupy 0-25% of the oropharyngeal width, 2+ is 26-50%, 3+ is 51-75%, and finally, 4+ 76-100%, in other words, the tonsils are almost touching at midline, called “kissing tonsils” [23]. 

Diagnosis/investigations:

When you have a patient you suspect has OSA, how do we confirm the diagnosis? The gold standard is formal polysomnography (poly som nog raphy), this involves monitoring the patients sleep patterns using a multitude of sensors including electroencephalogram, electro-oculogram, electromyogram, electrocardiogram, pulse oximetry, airflow, and respiratory effort, and must be done in a sleep lab [13,25]. However, (poly som nog raphy), polysomnography requires extensive resources, is inconvenient for the patient, and availability is limited in Canada. Therefore, at-home tests are often used in place of (poly som nog raphy), polysomnography. 

At-home tests assess fewer channels of data compared to those collected by (poly som nog raphy), polysomnography [13]. At home tests are inherently less accurate, but can be used to diagnose OSA along with a consistent clinical presentation. At-home tests can estimate the severity of OSA by recorded respiratory events including - apneas and hypopneas. Remember, as we discussed before, apneas are defined as a decrease of >/= 90% in respiratory airflow for 10 seconds or longer [5]. Hypopneas are defined as a >/=30% decrease in respiratory airflow for 10 seconds or longer with a >/= 4% decrease in oxygen saturation [5]. This is quantified using either the apnea index otherwise known as AI or the apnea-hypopnea index otherwise known as AHI [5]. AHI is the most commonly used. Diagnosis of OSA is made when the AHI is >/= 5 with daytime tiredness symptoms or comorbid cardiovascular disease; or it is diagnosed when the AHI is >/= 15 without associated symptoms or comorbidities [5]. AHI of 0-5 is normal aka no OSA, 6-15 is mild OSA, 16-30 is moderate OSA, and, AHI of >30 is severe OSA [5]. All symptomatic patients with even mild OSA should be treated, and patients with asymptomatic moderate to severe OSA should also be treated due to the health complications associated with untreated OSA.

The gold standard - polysomnography should be used when central sleep apnea or hypoventilation is suspected [2,13], or when OSA is still suspected, despite not being diagnosed with an at-home test, as at-home tests may underestimate the AHI [2,13]. Clinical suspicion is often used to guide management in pediatric patients and it is relatively rare to obtain a polysomnogram in children when OSA is suspected on history.

Some other techniques used to assess the location of obstruction in OSA include:

1. Muller's Maneuver, which is a physical exam/point of care maneuver where the patient is asked to make an inspiratory effort against a closed nose and mouth [26]. The degree of collapse is noted in the retropalatal and retroglossal areas [26].

2. Drug-induced sleep endoscopy (DICE): i) OR + sedation, ii) observe snoring and obstruction, iii) flexible endoscopy [27].

   • Advantages of this technique include that it allows for dynamic assessment sleep with direct visualization of involved structures.

   • Disadvantages of this technique include that it can only be done in the OR with an otolaryngologist under general anaesthetic. It is relatively specialized and isn't frequently done in general practice. Additionally, sedatives decrease muscle tone and respiratory drive and may artificially worsen OSA. 

Complications of Sleep Apnea 

So, why do healthcare providers and patients care to treat OSA? We’ve alluded to some consequences of untreated OSA so far, but let’s dive a little deeper.

Some complications of sleep apnea in adults include daytime fatigue, which of course can present with risks of its own, such as increased incidence of motor vehicle accidents [1]. Additionally, patients can experience an inability to concentrate, memory issues, and mood changes including irritability and depression [8]. In addition, cardiovascular problems, including hypertension are associated with sleep apnea due to the sudden decrease in blood oxygen concentration that can occur during sleep apnea [1]. Sleep apnea also increases one’s risk of developing Type II diabetes and metabolic impairment [8]. It is also important to consider the effect sleep apnea can have on the patient’s partner, including increased worry and stress, and sleep deprivation. 

Some complications of sleep apnea in children include pulmonary hypertension, behavioural issues, poor performance in school, and metabolic syndrome [12]. 

Treatment:

Now, how do we treat OSA to avoid these complications?

Treatment of OSA begins with a discussion of contributing social factors. One of the most significant factors is obesity. Reducing soft tissue through weight loss can result in significant benefits of AHI scores for patients [28]. Discussions about weight loss are sensitive and must be approached in a delicate fashion. It is important to discuss diet and exercise and consider setting SMART goals (which are specific, measurable, achievable, relevant, and time-related). Other lifestyle factors that may be addressed include sleep positioning, typically lateral decubitus position results in lower AHI scores compared with the supine position [17], smoking cessation, avoiding night time sedation (e.g. combining alcohol + sleep aids), and finally improvements in sleep hygiene. 

In general, the care of patients with OSA needs to be individualized. For some people, lifestyle modifications can take time to yield improvements and may not be sufficient to treat OSA on their own. Continuous positive airway pressure or CPAP is a common treatment option for OSA [17]. CPAP, as the name suggests, provides a continuous flow of air to the patient's airway; this promotes patency of the airway and therefore avoids the apneic and hypopneic episodes [29]. CPAP is shown to improve sleep quality, reduce AHI scores, and reduce the incidence of previously mentioned OSA complications [17,29]. There are a variety of masks to deliver CPAP and this is something that patients can discuss with their CPAP retailers [17]. Common patient complaints with CPAP use include difficulty getting comfortable for sleep, the mask falling off as they toss and turn in the night, and it being uncomfortable. Although many patients will adjust to this and find great benefit from use of nightly CPAP, compliance remains a significant downside of CPAP and is something that requires ongoing discussions with patients [17,30].

For patients who may not be experiencing benefits from CPAP or have difficulty tolerating it, bilevel positive airway pressure or BiPAP may be used, which exerts a higher pressure during inhalation and a lower pressure during exhalation [29]. Alleviating some discomfort with exhalation, especially if the patient is prone to hypoventilation. Other management options include auto-titrating CPAP which adjusts to deliver the minimal pressure to alleviate apnea and hypopnea episodes [29]. Oral appliances such as mandibular repositioning devices to maintain a patent airway have also been used, however, they are less effective than CPAP [17]. Oral appliances and medical treatments for nasal obstruction are also employed. 

Factors important in making the decision to treat OSA with a surgical procedure include the patient’s wishes, CPAP tolerance, severity of symptoms, severity of disease, patient comorbidities, and site and severity of upper airway collapse. Surgical interventions can be broadly divided into nasal surgery, palatal surgery and hypopharyngeal surgery. Surgeries such as septoplasties, and tonsillectomies aimed at improving different parts of a patient's airway have also been used as potential treatments for OSA. However, these are often not sufficient on their own, but may be used in combination with other treatments [17]. In particular, septoplasty has been shown to increase compliance rates of CPAP by reducing nasal obstruction, a common factor for CPAP non-adherence [31].

Uvulopalatopharyngoplasty or UPPP involves resection of excess soft tissue in the upper airway, including the uvula, soft palate, palatine tonsils, and excess pharyngeal tissue [31]. Despite it being the most popular surgical approach, the results are still not ideal with only an ~50% response rate cited at one-year post-operation [32,33]. Patients with low Friedman scores tend to have the best response to UPPP, whereas those with more severe oropharyngeal crowding tend to have a lower response rate to UPPP alone [21,34]. It is important to note that patient selection is the most important aspect in determining whether a patient is well-suited for CPAP. For example, literature has shown that patient selection for UPPP based on favourable anatomical factors significantly increases success rates, and is therefore an important aspect of a pre-operative consultation [34]. It is important to counsel patients on the variable outcomes of this procedure and that they may still be reliant on CPAP to fully resolve their symptoms and treat their OSA. 

Bariatric surgery for weight loss has been shown to be effective for reducing OSA severity, however lifestyle adjustments and CPAP remain a less invasive, yet effective treatment [35]. Finally, novel approaches to OSA treatment have been suggested, such as implanted hypoglossal nerve stimulators to increase the tone of the muscles which maintain the upper airway, although early evidence suggests successful results, more research is needed and these approaches remain more invasive than conventional treatment [36]. 

Lifestyle changes are first line treatment for OSA in adults, given the significant contribution of adenotonsillar hypertrophy to OSA in children, adeno-tonsillectomy is first-line treatment for pediatric OSA [9]. In fact, the cure rate in pediatrics is at least 90% with adenotonsillectomy! 

Intranasal corticosteroids aimed to shrink the adenoids have been used as medical management for pediatrics OSA [9]. However, outcomes can be variable, and compliance can be a challenge in this younger population. Therefore, this is rarely done and is not typically considered first line therapy.

Well that concludes our episode on sleep apnea! 

We would like to extend our sincerest thanks to the Saint John Regional Hospital Department of Surgery within the Horizon Health Network for their generous support. 

Thank you so much for listening to our podcast! We hope you’ll tune into our next episode!

Thank you to Kalpesh Hathi for leading authorship of this episode

Please head to our website at www.theotoapproach.com for our show notes, and to sign up for our newsletter to stay up to date with our latest episodes. 

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