Obstructive Sleep Apnea: The Impact on Swallowing in Adults

Editor's Note: This text is an edited transcript of the course Obstructive Sleep Apnea: The Impact on Swallowing in Adults presented by Kendrea L. (Focht) Garand, PhD, CScD, CCC-SLP, BCS-S, CBIS, CCRE.

Learning Outcomes

After this course, participants will be able to:

• Explain pathogenesis of OSA.
• Describe how OSA can impact swallowing function.
• Describe the current best evidence for managing OSA.

It's such a pleasure to return to speak on this interesting topic, or what I think is really interesting: obstructed sleep apnea, which I'll refer to as OSA for the rest of our time together.

I think we should first begin by defining what OSA is clinically. I always recognized that this was common in many of my patients' charts but never really thought much about it. I just assumed it was people who snored, and that was kind of it. Some of them used machines at night to help them not snore as much, and that was the extent of my knowledge.

It wasn't until my former doctorate student, Dr. Ankita Batata, came into my office one day when we were considering what she should research for her first project in the lab and her career trajectory. She mentioned that she had noticed an increase in referrals for instrumental assessments for swallowing, with the only diagnosis at that time being OSA.

I encouraged her to read more of the literature to better understand OSA and to start thinking about how it may impact swallowing.

What is OSA?

OSA is the most common sleep-related disorder. It's a breathing disorder, but it's sleep-related. It affects about 1 billion people worldwide, which is a massive number. The estimates are around 54 million people in the United States alone. OSA is characterized by the frequent or repetitive narrowing or complete collapse of the upper airway, such as the pharynx, during sleep.

The most frequent sites that tend to collapse in someone with OSA are the soft palate, the lateral pharyngeal walls, the palatine tonsils (if they have them), the base of the tongue, and even the larynx can be a site of obstruction in patients with OSA. This collapse will repeat throughout the night, causing fragmented sleep, and patients often report feeling really tired.

Why does the upper airway collapse? It can be due to a combination of anatomical and non-anatomical factors. Many of us are probably more familiar with the anatomical reasons, but for comprehensiveness, we will review both.

Anatomical Factors

Sticking to the anatomical factors, individuals with OSA often have a narrow or crowded upper airway, which can result from congenital conditions or genetic factors. For example, those familiar with Treacher-Collins syndrome or other syndromes with craniofacial anomalies can understand how these conditions lead to a crowded upper airway.

Another anatomical factor is an increased volume of soft tissues in the upper air digestive tract, which reduces the airway diameter. This can include increased volume in the genioglossus, pharyngeal walls, soft palate, and other areas. It's important to note that while OSA is often related to obesity, about 60% of patients who meet the BMI criteria for obesity do not have OSA. Conversely, lean individuals can also present with OSA, so there isn't a direct one-to-one relationship between obesity and OSA.

Lastly, OSA can be a consequence of the disease itself. Repeated snoring and trauma can result in edema of the upper airway tissues, further narrowing the airway and contributing to its severity.

Non-Anatomical Factors

Let's examine the non-anatomical factors. This was a completely new area of knowledge for me, especially when I read the literature to learn more. Individuals with sleep apnea tend to have a cyclical pattern of airway collapse during the night, as demonstrated by this graphic (See Handout, page 10). The individual with OSA will experience airway collapse, known as a hypopnea event or apnea event, leading to changes in blood gas volume.

Because of that, we're going to have an increase in carbon dioxide and a reduction in oxygen. This excites our sensory receptors, signaling that there's a change. We have these chemo or mechanical receptors that are activated by this alteration in blood gas volume, signaling the need to breathe. The excitation of these receptors arouses the individual from deep sleep, which is beneficial because it opens the airway and alters their breathing patterns. 

We can actually see individuals hyperventilate to increase oxygen levels and rebalance their blood gas volume. Unfortunately, this change in breathing predisposes them to experience more airway collapse when they return to sleep, and thus, the cycle repeats. In fact, for some individuals, this cycle of collapse and arousal can happen over 300 times in a given night.

Activity of Upper Airway. To describe the cycle of arousal and returning to collapse when an individual falls asleep, there's a reduction in cortical activity. There's a decrease in neuromuscular drive, including the drive that keeps the upper airway open for airflow exchange. This reduction increases the risk of airway narrowing or collapse, even in healthy individuals and especially in those with obstructive sleep apnea.

Patients with OSA demonstrate significantly reduced upper airway muscular activity during sleep, further increasing their risk of airway collapse. It's important to note that their pharyngeal muscles aren't necessarily weak; rather, there's a loss of neuromuscular drive at sleep onset, causing the collapse.

Interestingly, during wakefulness, patients with OSA have demonstrated increased upper airway muscular activity compared to healthy controls. This heightened activity is believed to be a compensatory mechanism for their narrowed airway, with the muscles working overtime to keep the upper airway open. However, this drive diminishes when the patient is asleep.

Summary of OSA Definition

Let's revisit our original question: Why does the upper airway collapse? In summary, it's a complex issue resulting from a combination of both anatomical and non-anatomical factors. This combination gives rise to the patient's obstructive sleep apnea, what we call their endotype.

While it's sometimes referred to as a phenotype, I believe "endotype" is a more accurate term. You may encounter this term in the literature or later in this course. What are the consequences of this repeated narrowing and collapse? First, it causes sensory-motor abnormalities in the upper airway. Patients with OSA may experience altered taste, smell, and blunting of various receptors, including chemo, mechanoreceptors, and thermal receptors. Additionally, changes in upper airway muscle fibers occur, transitioning from type one to type two muscle fibers. While type two fibers can generate more force, they are more prone to fatigue. These are common consequences of the repeating narrowing and collapse seen in individuals with OSA.

I find the Palm acronym (See Handout, page 11) useful for remembering both anatomical and non-anatomical factors. However, it's important to note that individuals can present with different combinations of these factors, leading to their OSA endotype. It's rare for an individual with OSA to only belong to one of these categories.

Why This Topic?

Now that we have a working definition of OSA and its pathobiology behind it, let's explore why I chose this topic. I would assume many of us know someone who has OSA or has treated patients with OSA on our caseload, perhaps as a comorbidity rather than the primary medical diagnosis leading to their referral. Consider how many patients have solely been diagnosed with OSA whom you've treated for dysphagia. So why is it clinically meaningful for us to no longer ignore this diagnosis?

OSA is a Health Crisis

OSA is indeed a major public health problem. We discussed the dramatic increase in prevalence, with 1 billion affected worldwide, and this prevalence continues to rise. The associated costs in the US alone exceed $12 billion annually.

Patients with OSA are at an increased risk for pneumonia, and this risk escalates with the severity of their OSA. While there's ongoing debate about the exact relationship between pneumonia and OSA, researchers are exploring factors such as reflux, aspiration, laryngeal dysfunction, and CPAP use.

OSA is also prevalent in conditions frequently seen on our caseloads, such as stroke, Parkinson's disease, spinal cord injury, and multiple sclerosis, all of which commonly present with dysphagia. Therefore, it's important for us, as speech-language pathologists, to consider the impact of an OSA diagnosis on dysphagia severity, especially in post-stroke patients.

For instance, does a premorbid OSA diagnosis potentially worsen dysphagia severity after a stroke due to existing sensory-motor changes? Furthermore, individuals with cardiovascular disease or progressive neurological disorders like Parkinson's may have undiagnosed OSA, affecting their dysphagia recovery and prognosis.

Dysphagia in OSA

A systematic review conducted by our team identified 17 eligible articles aiming to describe the prevalence of swallowing disorders or dysphagia specifically attributed to OSA in the literature. However, the reported prevalence varied greatly, ranging from as low as 16% to as high as 78%. This wide variability stemmed from several factors, including the definition used to categorize patients as having dysphagia—whether based on self-report, clinical examination, or instrumental examination.

This variability suggests that dysphagia in OSA is likely under-recognized and underreported. Considering that sensory alterations can result from the trauma caused by airway collapse during sleep, relying solely on patient reports of swallowing difficulties may miss many cases of dysphagia.

Among the most frequently reported swallowing impairments was delayed swallow initiation. However, it's worth questioning this classification, as the typical definition of "delayed" may not always apply, especially in cases involving larger volumes or sequential swallows of thin liquids, where the bolus may enter the pharynx before the initiation of the swallow—a phenomenon observed in healthy adults as well.

Airway invasion, including aspiration, was also noted, but it's essential to compare this to findings in healthy controls, as aspiration of pharyngeal residue can occur in both groups. Additionally, impaired respiratory swallow coordination was observed, characterized by introducing the swallow within the inhalatory cycle instead of the expected exhalatory cycle. These findings underscore the complexity of dysphagia in OSA and the importance of comprehensive assessment and understanding in clinical practice.

Survey Study

We also conducted a study to explore the knowledge, attitudes, and practice patterns among SLPs, particularly concerning the OSA patient population. Our aim was to determine whether SLPs know about OSA, their attitudes toward dysphagia management in OSA and whether they have patients with OSA on their caseloads. Perhaps some of you listening actually participated in the study, and if you did, we sincerely thank you for your contribution.

This study was conducted through an international survey to gather insights from SLPs across different regions and conducted at the height of COVID.  We had already been preparing it when our university shut down in March 2020, and we released the survey that same summer. Over the summer, we collected responses. To date, we believe we have the largest number of responses ever reported in the swallowing field, with input from over 800 clinicians. Almost all respondents were female, which aligns with the demographics of our profession. We had representation from over 20 countries, which was amazing, although most were from the United States, accounting for about 80% of the responses. 

Over 80% of respondents had a master's degree, which is not surprising given that it's an entry-level degree in the United States. Respondents came from various clinical settings, including acute care, inpatient rehab, and private practice. The majority, about 40%, were from acute care settings. Most clinicians were based in metropolitan areas and primarily worked with an adult caseload.

Okay, so what did we find? Overall, SLPs' knowledge about OSA—what it is, how it's managed, its definition, and how it's assessed—was relatively low, with an average knowledge score of around 55%. We used a highly validated questionnaire for this assessment. The knowledge scores ranged from as low as 14% to as high as 86%.

To give some context, this same validated questionnaire was used with non-sleep physicians, who scored between 60% and 77%. Interestingly, we found that experience with OSA had a significant effect on knowledge scores. Clinicians who had patients with OSA on their caseloads for a longer period were more likely to have higher knowledge scores, indicating a better understanding of what OSA is.

What were the speech-language pathologists' attitudes related to OSA? The majority of respondents indicated that identifying OSA in patients they treat is important. However, almost half were unclear about what their role should be when providing services to patients with OSA. Additionally, 20% disagreed that an SLP has any role in managing patients with OSA.

Interestingly, over half (about 66%) of the clinicians said that asking about OSA is important when gathering clinical history. This raises questions about why they ask about OSA and what they do with that information once it is gathered. Approximately half of the clinicians felt confident in managing dysphagia in this population, meaning the other 50% lacked confidence in managing dysphagia among patients with OSA.

Finally, regarding practice patterns, we found that just over half of the clinicians surveyed had patients with OSA on their caseload. This was higher than I anticipated, but given the high prevalence of OSA, it's possible that some patients are still being missed. About 60% of those referred for speech-language pathology services with a diagnosis of OSA were specifically referred for dysphagia services.

A limitation of this finding is that the referral for dysphagia services might not have been directly related to the OSA diagnosis. For example, a patient might have been referred due to a stroke but also had a diagnosis of OSA, which wasn't the primary reason for the referral. This detail wasn't captured in the survey, representing a limitation in our data. The Osaka questionnaire included questions related to the knowledge of what OSA is, how it's assessed, and how it's managed.

OSA Assessment and Treatment

Let's move on to how OSA is diagnosed and what the current medical management practices are before we discuss the role of SLPs. OSA should be diagnosed by a sleep specialist, typically a pulmonary and critical care physician specializing in sleep medicine. This often involves a comprehensive examination aimed at identifying risk factors.

These red flags can be suggestive that the patient may be experiencing OSA. These could be symptoms reported by the patients themselves or observations from their bed partner. Since an individual with OSA may not be aware that they have an issue during the night while sleeping, a physical examination is also performed. Let's look deeper into each of these components. Here's a quick summary of some common daytime and nighttime symptoms reported by patients with OSA, along with a discussion of sleep studies, which we'll cover in more detail.

Symptoms

These symptoms are critical for diagnosis. For instance, patients with OSA may complain of daytime sleepiness despite seemingly adequate sleep duration, or their bed partners may report loud snoring or observed instances where the patient stops breathing during sleep. Patients may also experience cognitive changes during the night, particularly affecting attention, memory, and mood, with symptoms of depression often reported. 

Fortunately, there are validated screening questionnaires that allow us to identify these risk factors quickly and easily. These questionnaires, commonly used in sleep clinics, can be administered in just a minute or two and are valuable for documenting changes before and after interventions are applied. They can be completed as paperwork prior to a scheduled appointment and uploaded into the patient's medical record. Some common screening questionnaires are the STOP-BANG and Epworth Sleep Scale. 

Physical Exam

In addition to trying to identify these red flags, the physician may also perform a physical examination. During this examination, they review key bodily systems, including the nervous, cardiovascular, and pulmonary systems. They also assess body mass index and measure neck circumference, and they may examine the upper airway for any anomalies, such as a recessed chin. They may also use tools to document how well the oropharynx can be visualized. For example, the Mallampati class was originally developed to assess intubation risk by looking at the oropharynx, but it has also been applied as a simple assessment tool for OSA. As you move between classes, fewer oropharyngeal structures are observed, with class four indicating only the hard palate is visible. Patients with a score of three or four are often considered to be at increased risk of having OSA. A diagnosis of OSA is typically confirmed through overnight in-lab polysomnography (PSG), supplemented by clinical history. These risk factors are considered the gold standard for diagnosing OSA.

Here is an example (See Handout, page 20) of the recordings obtained during a sleep study.  I actually had a sleep study performed, and it was quite fascinating being hooked up to all these machines and undergoing what our patients experience themselves. During a sleep study, sleep stages are recorded using various methods. EEG electrodes are placed on the scalp to monitor brain activity, while EOG electrodes monitor eye movements, and chin sEMG electrodes track muscle movement. Additionally, sEMGs are placed on the legs to monitor leg movement, and an EKG monitors heart rhythm. Measures related to breathing include a cannula to detect airflow from the nose, bands on the chest and abdomen to monitor movements associated with breathing, and finger monitoring for peripheral oxygen saturation levels. Video monitoring during sleep allows sleep technologists to observe sleep-related behaviors, such as talking in one's sleep or sleepwalking, as well as sleep positions and duration.

The sleep physician then analyzes all these measures, usually the next day, to determine whether sleep behaviors are considered "normal" or "abnormal."

OSA Severity

A key aspect of monitoring during a sleep study is analyzing the breathing pattern to detect the presence of apneas and hypopneas. A true obstructive apnea is defined as the cessation of airflow for at least 10 seconds, followed by persistent respiratory effort. The Apnea-Hypopnea Index (AHI) is calculated by dividing the number of hypopnea events by the total number of hours of sleep. OSA is diagnosed when the derived AHI score is greater than or equal to five events per hour of sleep. Severity classifications are based on AHI scores that are described here (See Handout, page 21), with higher scores indicating a more severe OSA disease state.

However, the AHI has its limitations. It fails to account for the duration of each event, and there can be variations in individual responses between nights and among patients with the same AHI disease severity. Additionally, events lasting less than 10 seconds are still concerning and are included in the calculation of the AHI. This operational definition of hypopnea includes any airway narrowing lasting less than 10 seconds.

The 10-second criterion is based on what is considered normal for healthy individuals during sleep. A cessation of airflow beyond 10 seconds would be considered abnormal for individuals without symptoms.

Treatments

The treatment options for OSA that the healthcare team may recommend are depicted here (See Handout, page 22). They are divided into two major categories: non-surgical and surgical treatment options. Let's first focus on the non-surgical options, which are more prevalent, specifically non-invasive ventilation. 

Non-Surgical Treatments. Our non-invasive ventilation, which you might hear called NIV, includes CPAP, which stands for continuous positive airway pressure. CPAP is the first line of treatment. During CPAP, positive pressure is delivered via a mask, and this continuous positive pressure helps keep the upper airway open.

Because of that, it helps prevent collapse. This has been shown to work, but non-adherence (I'm not going to call it compliance) to CPAP is reported to be as high as 50% in patients. Think about it: if 1 billion people have OSA, that means 500 million people are choosing not to use CPAP. The most common reasons for not using it include feelings of claustrophobia from the mask, discomfort while wearing it at night, and complaints of dry mouth.

Other complaints exist as well. Oral appliances, which help keep the tongue from falling back (the back of the oral tongue, not the base of the tongue) into the oropharynx, or devices that advance the jaw forward (called mandibular advancement devices or mandibular repositioning devices), may be recommended. These are options for patients who might not pursue CPAP or for whom surgical options are inappropriate.

Again, the whole point is that you're moving the structures out of the way to help improve upper airway patency during sleep. There are also what we call adjuvant therapies, more on the behavioral side. For instance, if a patient has a higher BMI, a weight loss management program might be recommended. Additionally, adjusting the sleep position, such as lying on one's side, can be advised.

Typically, these aren't standalone treatments. It's often a combination of CPAP plus a weight loss management plan. However, adjuvant therapies may be used or recommended alongside other treatment options listed on this slide. Due to the high rates of non-adherence with CPAP and the substantial healthcare burden it poses, particularly the increased financial cost of OSA management, there has been growing interest, especially in the past 5-10 years, in exploring other therapeutic options that are non-CPAP. These options aim to alleviate reported symptoms and the severity of OSA itself. Examples include oral-pharyngeal exercises, also known as orofacial myofunctional therapy or OMT, and respiratory muscular strength training (RMST). We'll delve into these specifics shortly, as they are particularly relevant to what we do as SLPs.

Surgical Treatments. For more severe cases, surgical options may be considered and divided into different phases. Phase one surgeries typically involve removing structures contributing to airway obstruction, such as enlarged tonsils or adenoids. These surgeries may be performed in combination, addressing multiple obstructions. If patients don't benefit from phase one, they may proceed to phase two surgeries. These are for individuals with significant velopharyngeal obstruction, involving more extensive procedures.

Recent literature has emerged on hypoglossal nerve stimulation. This nerve, the 12th cranial nerve, innervates intrinsic and some extrinsic lingual muscles. Stimulation aims to prevent upper airway collapse by promoting lingual protrusion, helping maintain airway patency during sleep. To achieve this effect, an implantable device is attached to the hypoglossal nerve.

Behavioral Treatments in OSA

Returning to behavioral interventions, exercises targeting the head, neck, and respiratory musculature are gaining attention. It's worth noting how aging intersects with our next topic. Oral pharyngeal exercises, which target articulatory structures of the head and neck, have gained attention in recent years, particularly in regions like Brazil, Turkey, and parts of North America.

Oromotor therapies (OMTs) involving exercises for the jaw, tongue, lips, and related structures have emerged as potential treatments for obstructive sleep apnea (OSA). These exercises aim to enhance muscle tone and endurance, potentially reducing the risk of airway collapse during sleep. However, determining the most effective exercises and their appropriate dosage remains challenging due to variations in research findings.

Studies on oromotor therapies for OSA have explored various exercises such as lingual resistance exercises, lip range of motion exercises, chewing exercises, and articulation drills. However, findings from these studies are mixed, and there are significant methodological concerns. For instance, there's uncertainty about how these exercises effectively prevent pharyngeal collapse. Additionally, subjective outcome measures and potential placebo effects can influence reported improvements, making it challenging to determine the true efficacy of these interventions.

Respiratory muscle strength training (RMST) has garnered interest, particularly in inspiratory muscle strength training (IMT), with more studies supporting its efficacy. However, there's growing attention to expiratory muscle strength training (EMST) as well, albeit with fewer studies. The rationale behind EMST lies in improving coordination between the lower and upper respiratory systems to prevent collapsibility. By strengthening expiratory muscles, the aim is to override obstructions and enhance airflow. While evidence remains mixed, patient reports often indicate improved sleep quality due to RMST.

Subjective measures have shown some support for respiratory muscle strength training (RMST), but findings remain inconclusive due to conflicting study results. While some studies suggest improvements in AHI disease severity scores, there's a notable lack of research on swallowing-related outcomes in this context.

Dysphagia in OSA

Our review indicated that patients with OSA frequently experience swallowing impairments, as evidenced by patient-reported outcomes such as the EAT-10, instrumental exams like modified barium swallow studies (MBS) or fiberoptic endoscopic evaluation of swallowing (FEES), and high-resolution pharyngeal manometry (HRM). Additionally, research has highlighted an elevated risk of aspiration pneumonia among individuals with OSA, although the underlying mechanisms are intricate and complex.

While dysphagia likely plays a significant role in the development of aspiration pneumonia in OSA patients, it's important to recognize that they are also susceptible to other comorbidities, such as stroke and Parkinson's disease, both of which can also lead to dysphagia. This complexity underscores the need for a comprehensive understanding of the interplay between OSA, dysphagia, and associated morbidities, rather than a simplistic one-to-one relationship.

Causes of Dysphagia in OSA

OSA contributes to swallowing impairments through several factors. First, the vibratory trauma caused by snoring and the collapse of the airway during apneic events can lead to sensory motor alterations. This trauma, combined with reduced or absent airflow during apneic episodes, can cause inflammation and stretching of pharyngeal tissues, resulting in further narrowing of the pharynx.

Additionally, patients with OSA may experience altered central respiratory swallow integration, leading to changes in the respiratory-swallowing pattern. Swallowing, occurring predominantly during the inhalation cycle, can contribute to unsafe and inefficient swallowing.

These alterations not only contribute to swallowing impairments but may also exacerbate upper airway dysfunction, further worsening the severity of OSA. It's important to recognize the complex interplay between these factors rather than viewing them in isolation.

A study found that patients with dysphagia required higher CPAP pressures to maintain airway patency. This may be due to the collapse of the base of the tongue, resulting in reduced muscle responsiveness of the genioglossus, an extrinsic lingual muscle involved in tongue protrusion.

Reflux in OSA

Considering reflux alongside dysphagia is critical, as they often coexist. A meta-analysis revealed reflux prevalence in nearly half of OSA patients. This reflux is attributed to increased negative intrathoracic pressure, facilitating gastric content migration into the esophagus and potentially the pharynx. Consequently, reflux-induced inflammatory changes in the upper airways may lead to tissue thickening and narrowing, exacerbating OSA severity.

While the full relationship remains unclear, their study observed dysphagia in approximately one-fifth of patients with moderate to severe OSA who also had reflux. This underscores the intertwined nature of OSA, dysphagia, and reflux, necessitating comprehensive evaluation and management.

Dysphagia Management Considerations

The management of dysphagia in OSA parallels approaches in other populations, involving comprehensive assessment and targeted interventions. However, OSA's unique influence on the upper airway prompts considerations of its impact on swallowing function. Sensory-motor abnormalities and potential endurance issues due to fiber-type shifts are among the factors to address.

In therapeutic targeting, objectives include enhancing upper airway sensation, maintaining airway protection, and optimizing respiratory swallow coordination. Tailoring treatment to address specific impairments is paramount. In our research, we're exploring the application of respiratory muscle strength training to rehabilitate swallowing and airway clearance capacity in patients with moderate to severe OSA, with promising preliminary data awaiting presentation.

EMST Study

We're about to move into looking at untreated OSA patients specifically for our work. We're just focusing on EMST right now. We believe that by improving neuromuscular adaptations and upper airway sensations, we can enhance swallowing safety, efficiency, and airway clearance. So, this is our preliminary study.

I was really hoping it would be published by now, so maybe it will be available in another month. I'm sorry for the delay. We worked with ten patients. We collected pre-intervention EMST data and then immediate post-intervention data. We used the EMST 150 device, setting it at 75% of its maximum expiratory pressure, which is consistent with our clinical practices for other interventions.

These patients participated in either telehealth treatment sessions or weekly in-clinic visits. Each week, we reset their new threshold. We used the EAT-10 and the Reflux Symptom Index (RSI) for assessment and conducted pre- and post-modified barium swallow studies. All patients completed the study with 100% adherence to the protocol. Although OT and PT values were higher than normative values, there was no significant difference between this group and others.

I want to mention that all these patients were using CPAP every night for a minimum of 7 hours. Approximately 60% of their swallows deviated from normal reference values when looking at biomechanical measures, such as timing and distance measures for critical pharyngeal events like time to laryngeal vestibular closure and hyoid movement. Following EMST, we observed increased proportions of these values returning to normal, which is a positive finding. However, the degree of change did not reach statistical significance, which was not unexpected given the small sample size of ten patients. Maximum expiratory pressures increased significantly, which is what we aimed to target with the expiratory muscles.

We also observed moderate gains in peak cough flow. When examining pharyngeal total scores, we identified five treatment responders—meaning individuals who showed a meaningful change in their scores. Notably, four of these five responders demonstrated significant improvements, specifically in tongue base retraction during swallowing.

However, there are some limitations to our study. We did not have a control group, all participants were being treated with CPAP, and our sample size was small. Additionally, we did not account for the underlying reasons for their upper airway collapse.

Summary

Overall, we know OSA is the most common sleep disorder. There are both anatomical and non-anatomical factors contributing to the presence of upper airway collapse, and more likely than not, your patient is going to have more than one of these factors. Dysphagia in OSA is poorly understood, likely underreported, and underrecognized. Evidence has demonstrated that there are sensory motor changes resulting from the upper airway collapse.

Evidence is currently lacking for how to best manage these patients. We don't know if their treatment response is dependent on their OSA endotype or phenotype, or their specific expression of swallowing impairments. In swallowing rehab, none of us know the optimal dosage. For the EMST study, we followed the "fives rule" of five reps equal a set, five sets per day, five days per week, and we did it for a period of time.

We were not as focused on strengthening the muscles as on improving endurance. However, there are dosage parameters that separate strength training from endurance training. Additionally, EMST is nonspecific; patients are not engaging in swallowing during the exercises. So, how can we work on the skill of swallowing itself? Maybe combining an exercise-based paradigm with direct swallowing practice could be more effective.

So I bet we're going to see more and more research related to dysphagia and OSA because I think there's been increased awareness and effort to support these investigations. As I mentioned, we were doing EMST treatment in patients who were treated with CPAP. We are about to start performing EMST in untreated OSA patients, those who are not on CPAP.

But what can we do now, right? You may have a patient on your caseload right now who has OSA. So, it's important to ask if your patient has OSA, especially for a neurogenic population, such as those with stroke, Parkinson's, etc. We may have these sensory-motor abnormalities resulting from OSA itself, in addition to other abnormalities from the primary disease process. This can impact their dysphagia presentation, severity, and even prognosis.

Maybe you can start implementing one of those sleep apnea screening measures, like the STOP-Bang questionnaire, if you suspect the patient may have undiagnosed OSA. This can help refer them for proper management. I believe we play a crucial role in referring patients to sleep physicians and being an active part of the sleep clinic process. We may not need to be in their clinics, but it's vital that they know we're available for referrals if needed.

Make sure you know who your sleep physicians are, establish a good rapport, and develop a clinical decision tree to help identify patients who may benefit from your services. As an SLP, stay updated with the literature on therapies appropriate for managing dysphagia and OSA. There might even be a role in providing prophylactic swallowing exercises for this population.

Consider what we do for head and neck cancer patients, keeping up a functional reserve. If they experience a stroke or Parkinson's onset, they’ll have a better functional reserve to address those challenges.

Questions and Answers

Is there a correlation of OSA with LPR or GERD?

Yes, absolutely. They just don't know what causes what. So they don't know if the OSA was present first, and that led to those intrathoracic changes which allowed the gastric content to escape. Or does the GERD come first? That leads to the inflammatory response, which then causes OSA. It's probably cyclical. They probably play off each other.

So, if you have a patient with OSA, I would screen. You can use the Reflux Screening Index or something similar because it may also need to be medically managed, or you can offer some behavioral strategies to reduce the impact of reflux. 

Are there specific types of OSA, some of which are less obstructive than others? I've heard that one is more common among women.

Yeah, so I was kind of hinting at that. That's a great question about women. This started getting some attention when we started finding that you did not have to be "obese" to have OSA. There were patients with lean muscle mass who were showing up in clinics that were found to have OSA. Some of them were perineal, postmenopausal women. So, they weren't morbidly obese, but they were found to have OSA. There has been an interest in figuring out, especially for postmenopausal women, how those hormonal fluctuations or changes at that time would contribute to some of these kinds of non-anatomical factors resulting in the presence of OSA.

Do you have any ideas about how to write a goal for this?

Yes, you would write the goal just like anything else because you should remember your role as an SLP.  You're not fixing the OSA, right? What you're trying to do is fix the potential consequences resulting from that. So, you'll still write your goal like you normally would for any patient population. For example, if you are targeting improvement in airway clearance capacity, if you're targeting improvement in tongue contact with the posterior pharyngeal wall, you are still writing your goals. If you want to make sure the patient has been educated and can articulate back to you behavioral strategies to reduce the incidence of reflux, that's your goal.  Whatever it is, keep it to what you would normally do. As I said, we are never targeting the disease process. We don't get paid enough for that, but we do target the consequences of it. 

Are both episodes of hypotension and apnea given equal weight in the calculation? 

It's just a summary score. You're just adding the hypopnea and apnea. You're not breaking it down into a portion of what contributed the most

Is upper palatal expansion still being used to treat OSA?

In my clinical experience, no. But I don't know if that's physician, clinic, country, or geographic dependent. Patients who undergo more extensive surgeries are also still pretty rare. Most of your patients will go under CPAP and maybe remove the tonsils and adenoids, but anything related to palatal expansion is not being used in my clinical experience. 

How do physicians determine the cause of OSA if a tongue retraction device that might work with a CPAP isn't something the patient can comply with?

This goes back to figuring out the endotype of those patients. So what is contributing?  If they know that the portion of their airway is being obstructed because the tongue is in a more posterior placement, then that would allow them to try surgical options or the mandibular advancement devices to ensure the tongue is in a more anterior position. So that can be done because one thing that can be done during a sleep study is that they can actually put in a pharyngeal catheter to monitor pressure and determine where the sites of extraction are actually occurring.

How does a recessed chin increase the risk?

Your tongue is anchored to your lower jaw, the floor of your mouth. If my mandible is recessed more posteriorly, that's also bringing those structures more posteriorly. Thus, you can have an airway collapse. Think about children with Pierre Robin syndrome, they are likely to have that recessed jaw. They are likely then to have an obstruction in the pharynx because of that.

Do personal sleep monitoring devices, like Fitbit watches, give any indication of OSA?

My father has OSA, and he's on CPAP. He uses it every night; for him, it is night and day. He wonders why he didn't do it years before.   So, can they give any indication of OSA? Yes, I think they can. The physician will still depend on what is being told. 

There are at-Home Sleep Testing (HSAT) devices. They could even be a watch you put on, similar to a pulse oximeter on your finger. Sometimes, they come with bands that are really easy to put on. The device collects data for several nights in a row, which is sent via Bluetooth via an app on your phone to be reviewed by a sleep specialist.

References: See handout for full list.