The US and global impact of Obstructive Sleep Apnea (OSA) is staggering. An estimated 52 million Americans have sleep disordered breathing, with 1 in 5 having mild apnea, and 1 in 15 having moderate to severe apnea. To quote Dr. John Remmers, “Obstructive Sleep Apnea is the most common non-communicable disease in the western world with over 200 million apneics and approximately 20 million new cases identified each year.” In the US in particular, that’s more patients than can possibly be treated with current available resources. It’s therefore imperative for all practitioners involved with Sleep Apnea management to unify – sleep physicians and sleep dentists. We need to think about ways to best serve our patients, because this is a problem that’s not going away.
Briefly about my background: I’m boarded both in Internal Medicine and Sleep Medicine, was diagnosed with OSA in 2000 and have been a compliant CPAP (Continuous Positive Airway Pressure) user ever since. In 2004, I was recommended to try OAT (Oral Appliance Therapy) as an alternative to CPAP. Unfortunately, this turned out to be a bad experience resulting in my rejection of oral appliances for some time. The failure of that appliance was, in retrospect, both my fault (for not being more proactive in voicing discomfort issues) as well as the sleep dentist, who was not vested in the appliance’s overall success. As a result, I was quite disinterested in oral appliances for many years. It took the realization that patients would be better served if they were offered an alternative to CPAP, namely oral appliances, and that actual CPAP compliance, even with coaching, was far from perfect. I also learned valuable lessons in treating patients with oral appliance therapy and some pitfalls to avoid.
OSA can have a profound impact our patients, whether they are aware of it or not, with numerous associations between sleep apnea and Cardiovascular diseases, including Stroke, MI, A fib, Diabetes and Hypertension. For example, 80% of Resistant Hypertension patients (defined as 3 or more BP meds with persistent BP elevation) have sleep apnea. Approximately 50% of patients with Atrial Fibrillation have sleep apnea. The combination of obesity (BMI>30) and Type 2 diabetes poses a 90% chance of having OSA. Another way to look at this is that the obese diabetic patient has a 1 in 10 chance of NOT having sleep apnea. In addition to OSA’s strong association with common diseases, we have numerous studies demonstrating adverse outcomes in OSA patients. In the Wisconsin sleep study, severe sleep apnea was associated with reduced life expectancy of approximately 7 years. In the Bussleton Health Study (which published 20 yr. follow-up data in 2014), patients that had untreated moderate and severe sleep apnea had a higher all-cause mortality rate, higher stroke rate and higher cancer rate than patients who either had mild OSA or no OSA at all. This data collectively makes the diagnosis and management of OSA not only an imperative, it obligates us to impress upon all OSA patients the necessity of continued therapy, usually indefinitely.
Despite much improved compliance rates with OAT vs CPAP therapy, both therapies still suffer from significant discontinuation rates that are at least partially our fault (both Sleep Physicians and Sleep Dentists). From my perspective, at least part of this compliance issue stems from patient expectations and general misunderstanding of the importance of treatment. In the past, patients, and even practitioners, have made the mistake of presuming that sleep apnea is snoring and daytime sleepiness. This creates a problem for future management if a patient has neither apparent daytime sleepiness nor obvious snoring. Regardless of symptoms and signs, untreated patients with significant apnea run the risk of future cardiovascular events and must be treated. Most of the CPAP cardiovascular outcome studies (which are plagued by poor compliance) enrolled mostly non-sleepy OSA patients. The analogy of Hypertension is a simple but accurate one, that can be utilized in the Sleep Apnea arena. The majority of patients with Hypertension understand they need to be treated if their blood pressure is high, regardless of symptoms. Continuation or discontinuation of therapy is not a real choice. Because of a lack of a clear-cut association between elevated blood pressure and symptoms, Hypertension has been deemed “The Silent Killer.” Management of sleep apnea should be thought of in a similar way. We should impress upon our patients that we are treating sleep apnea, also a silent killer, because of the cardiovascular ramifications, and not solely to improve symptomology. This seems obvious, but often falls short in clinical practice. I would suggest that we clearly communicate to our patients that it is an imperative to eliminate apnea to the best of our abilities, with the secondary goal being improvement in symptomology. Unfortunately, all too often we are focusing on the latter and forgetting about the former. This leads to dissatisfaction and poor compliance and a somewhat laissez-faire attitude about all available therapies, including oral appliance and CPAP therapy. I’ve seen numerous patients over the years that sheepishly admit that they’ve discontinued CPAP or OAT, but without the connection that this would be as bold as discontinuation of their blood pressure therapy. Because of the lack of obvious worsening from discontinuation of OSA therapy, and the frequent lack of correlating any change in quality of life with lack of therapy, patients are confused about the necessity of compliance. I recently saw a patient for routine follow up who complained that he had a major increase in frequency of nocturia (from 1 time per night to 3 times per night). When asked about his CPAP/OAT compliance, he chortled that he stopped using both approximately 3 months before, but was blissfully unaware that the worsening of nocturia was probably related to discontinuation (improvement in nocturia is often a harbinger of OSA therapeutic improvement). The association between untreated OSA, the subsequent rise in nocturnal ANP (Atrial Natriuretic Peptide), and a resultant increased nocturia, has been well described. But the majority of patients and clinicians are unaware of this phenomenon. Far too often patients view OSA therapy as a nuisance and fail to recognize that untreated OSA causes measurable insults to their bodies. It’s for that reason that I’m a firm believer in imparting some of the basic pathophysiology of OSA to all my patients in the hope that they will think twice before avoiding therapy each night.
OSA’s impact on the body comes in three forms – Sleep Fragmentation, Increased Adrenergic Tone, and Repeated Hypoxic Episodes. The first, sleep fragmentation, is not unique to OSA but can be seen in other sleep disorders such as RLS. The brief arousals that follow apneic episodes (as well hypopneas and RERAs) are protective in restoring CO2 and Oxygen levels but cause interruption in sleep continuity which may or not translate into daytime symptoms, including EDS, grogginess, poor concentration and memory, and irritability. The association between daytime symptoms and the degree of sleep fragmentation often doesn’t correlate (described by Chervin and others), but the general rule would be the more the fragmentation, the greater degree of impairment. As a cautionary note I would suggest not relying solely on daytime symptoms to guide diagnosis and therapy. The second feature that drives OSA pathophysiology is repeated brief episodes of increased sympathetic tone during apneic episodes, first described by Mignot in the early 80’s, which leads to alpha vasoconstriction, and eventually increased daytime sympathetic tone. This increased sympathetic tone is at least one of the driving forces in OSA’s association with HTN, CVA, A-fib and even Insulin Resistance and Diabetes. Repeated drops in oxygen (which in most OSA patients are not severe) has been associated with increased inflammatory response. The associations with both Cardiovascular Disease, Diabetes and even Cancer seem to be driven in part by chronic inflammation. Three entities are hallmarks of successful OSA therapy: Decreased Sleep Fragmentation, Decreased Adrenergic Tone and Decreased Hypoxic episodes. And it’s these three things that I attempt to remind patients of so that they can make rational decisions in regards to their care.
But cogent words alone don’t always shape behaviors to a satisfactory degree, and many patients and clinicians will be frustrated and mystified that despite good compliance with OAT and or CPAP therapy, they don’t feel hugely different. It is therefore important for us as sleep clinicians to think about the whole gestalt of sleep. This includes stressing good sleep hygiene, circadian alignment and even diet and exercise.
As a resident in training, I was introduced to the concept of Good Sleep Hygiene by a forensic psychiatrist who believed strongly that all patients should be aware that their overall wellbeing can be influenced by sleep habits. At first, I was reluctant to embrace this and believed that good sleep hygiene was a bromide platitude, obvious to most people. But over the years it is amazing how powerful reinforcement of good sleep habits can be, especially when you’re passionate about it. Use it like a prescription. Shutting off electronics before bed, not getting into bed until you’re ready to sleep, avoidance of caffeine after 2 p.m., avoidance of alcohol close to bedtime, and having relatively the same wake time, to name a few, are easy to initiate with rapid results. I always tell my patients and non-sleep colleagues that the secret to regulating sleep is not the time you go to bed but the time you wake up. Simply put, if someone is forced to wake up every morning (7 days per week) at the same time, and not allowed to nap, they will have tremendous sleep drive in the evening that can minimize issues with sleep continuity.
It’s important to remember with sleep patients that there are many factors that can impact how patients feel overall. The long-term success of oral appliance and CPAP therapy is not only contingent on reducing and or eliminating obstructive events, but is also dependent on improvement in sleep quality. Sleep quality is a somewhat nebulous construct with multiple elements making direct or indirect contributions including sleep architecture, undocumented sleep fragmentation, sleep continuity, sleep efficiency, circadian alignment, and of course sleep duration. As a sleep dentist, you must have some understanding and comfort level in this area if you wish to have long term success and retention of OSA patients.
It’s important to remember that sleep quality and sleep apnea are often unrelated. An example is the lack of improvement in AHI with nasal patency devices, despite improvements in sleep quality. Or the supposition that if an OSA patient begins remembering dreams after OAT that this necessarily reflects objective improvements in the AHI.
In addition to good sleep hygiene and sleep quality, a crucial, but often overlooked factor is sleep duration. Short sleep duration is by far the most common reason for daytime sleepiness, and although there’s much debate about the actual requirement for health, most individuals require between 7 and 8 hours of sleep. It’s necessary to stress this to patients since use of any OSA therapy in someone with self-imposed sleep restriction will often have minimal to no abrogation of their symptoms, nor any benefit of therapy. Terry Weaver, RN, PhD, showed that Moderate to Severe OSA patients who used CPAP for less than 6 hours a night had evidence of objective and subjective daytime sleepiness. Those who used it for only 4 hours or less were no different from baseline (prior to therapy). The recommendation to increase sleep duration from the sleep clinician can improve your patient’s quality of life, feeling of restfulness, and perceived wellness.
There is a great opportunity for all of us in the field of sleep to have a major impact on our patients’ health. As our OSA patients adopt some simple rules and concepts, we can not only improve treatment efficacy, but they will feel improved quality of life. Together, we can potentially improve their morbidity and mortality, which is tremendously rewarding and very powerful. We need to stress the importance of treatment in terms of the broader picture and not focus on only improving symptoms. Both the Sleep Dentist and the Sleep Physician must speak with one unified message.
