In Part I, we ran through a few examples comparing something as obvious as heart disease and the full insurance coverage often provided for related cardiac care to the problem of sleep disorders, in particular sleep apnea, and the general lack of interest and specific lack of coverage in promoting greater use of CPAP. In the zero sum game of healthcare, sleep medicine is increasingly looking like an imminent loser in so far as services are continuously downgraded to a point where patients either adapt to the PAP machine rapidly or the device is withdrawn. The epitome of such a model of care would be undergoing HST, then receiving an APAP device, and then when some proportion of patients struggle after say one month, insurance coverage ceases. The patient can always try again, but in this model, the general belief would be the patient just is not sufficiently motivated to regularly use PAP and therefore any additional insurance coverage is not a worthy expenditure of time, money and resources.
While this approach looks irrational if you know a lot about sleep apnea and the benefits of its treatment, an insurance company’s perspective revolves around the “use it or lose it” paradigm. Currently this view is entrenched among most carriers, because it appears to make a great deal of economic or financial sense. And, it could be reasonably argued that this big picture approach is actually based on a very practical tunnel vision in light of the vast numbers of CPAP users who give up.
In fact, from the above description of the problem of maintenance of use among CPAP patients, it is much more understandable that these businesses would have developed policies to utilize prior authorizations for testing in the sleep lab.
Let’s begin at the beginning of the HST/APAP model and see how it suits the insurance companies’ rationales and policies. Then, I will attempt to show why this model actually hurts the insurers more than they realize.
The basic premise about CPAP use, widely held by many in the field including sleep doctors and techs, sleep center staff, and many other indirect providers of care who engage with OSA/UARS patients, can be succinctly defined as simply as “most people do not want to use CPAP or most people cannot use it.” In other words, across virtually all spectrums of patients, patient care resources, physicians, DME companies, government regulators and health insurers, the belief is that the average patient just will not or cannot use PAP therapy. This belief does not propose it is impossible to use PAP or that there are not lots of people benefiting from PAP. Rather, this belief is the conventional wisdom that subscribes to the facts on the ground where so many more people appear to struggle with PAP compared to those who take to PAP likes ducks to water.
Somewhere between the serious strugglers and the avid users lies a middle ground comprising a vast number of individuals with variable degrees of use and variable degrees of benefit. Obviously, this middle ground does not include OSA/UARS superstars who can implement PAP all night every night within the first week or two of use and easily achieve hours ranging from 6 to 9 per night. These superstars are perceived by the medical and health industry as accounting for only one-third, at best, of PAP attempters and ultimately users. So, while there are many who flatout quit within a few days, the middle grounders look much closer to quitters than superstar users.
With this thumbnail sketch of general PAP use, you can see that the people who pay for the coverage of PAP equipment must be feeling like they are losing a lot of time and money when so much effort is invested in as many as two-thirds of patients who might never become truly regular and diligent users.
What would you do in their circumstances? Would you keep pouring more coverage money into the pot in the belief user rates will eventually rise to a level of cost-effectiveness, or at some point, wouldn’t you become suspicious about the whole PAP line of treatment? Wouldn’t you in fact want to find a way to rather quickly weed out the winners (users) and losers (quitters) so that you could invest your coverage money towards those inclined to stick with the program?
If you think about how an insurance company survives in the real world of healthcare, then prior authorizations would at first glance make a great deal of sense. Below is a brief list of some of the obvious reasons an authorization system would cut losses.
First and foremost, if the insurance company uses strict criteria, it can reject almost anyone from ever returning to the sleep lab. What in fact are the most common reasons someone needs to return to the lab? The answers fall into only a few categories: persistent mask fit difficulties, intractable mask leak issues, unresolved leg jerk issues, and a poor response to PAP therapy due to either the wrong type of device or the wrong pressure settings. There are variations on all these aspects of PAP therapy, such as chronic mouthing breathing and dry mouth, but both these problems are usually related to mask issues or the use of a chinstrap or mouth taping.
Thus, if we look at each of these factors, how essential is the lab environment in resolving them? From a pragmatic point of view, a patient could make repeated trips to the DME provider or to the daytime sleep center staff to be fitted and to receive a new mask to attempt to resolve all mask issues. For the problem of leg jerks, the patient could be tried sequentially on multiple different medications or supplements or both over a period of weeks and months until the patient reports enhanced sleep consolidation and a resultant improved response to PAP. Last, regarding the PAP device itself, the patient could be sequentially switched from CPAP to APAP, and then to BPAP, and then perhaps even ABPAP. After a trial with each new device, the patient would return for a data download and discuss progress, at which point the provider, physician or sleep technologist adjusts the pressure settings based on the information acquired in the data download.
While all the above seems pragmatic, it turns out to be erroneous on several fronts, but we’ll get to these fallacies in the subsequent post. Let’s imagine for the moment there are no other options, as is the case nowadays with many sleep centers restricted by insurance policies prohibiting or severely curbing sleep lab use. From the insurance companies’ viewpoint, these sequential interventions are not that expensive (especially if the DME creates a PAP device loaner system) and could lead to either success or failure. Most of the time, the results are a mixed bag, because these processes take too long for the average patient to maintain interest or motivation to continue. In other words, a huge proportion of patients drop out of care anywhere along this timeline, because what’s usually happening is a worsening of sleep, which in turn kills motivation within a matter of days. Theoretically, acceptance of this fact (of early failure) is more than acceptable to the insurers, because they believe these patients returning to the sleep lab would never have transformed them into satisfied customers who regularly us PAP.
It is important to note the insurance company does not perceive itself as doing anything wrong or evil. It is persuaded that PAP patients are mostly losers (quitters), and they don’t want to foot the bill. If they enact tough authorization systems, it never occurs to them they are harming their patients. What occurs to them is that they are not only saving money for the company, but they may also be helping patients recognize sooner than later that PAP therapy is not a good treatment option for them. Though this logic seems somewhat twisted, the insurers merely need to look at most of the adherence data about PAP in the scientific literature to be persuaded they are on the correct side of the argument. Again, if insurance companies put too much money into a losing proposition, then they go out of business and all their customers lose out not just the sleep apnea patients.
Do you see something clearly wrong or obviously illogical with these lines of thinking? The most rational concern is whether or not the above mentioned problems actually can be fixed sooner or more effectively by returning to the sleep lab, thus cutting down the timespan between first starting with PAP and then appreciating actual treatment gains and benefits. And, even more importantly, is there something about returning to the sleep lab that turns things around such that the patient reports sleeping better?
This concept of “sleeping better” is unbelievably critical to this discussion, so permit me to delve into its meaning and its impact on patient care. To start, consider our previous discussions about the Ceiling Effect, where with every improvement in sleep quality, the individual patient often appreciates things have gotten better, however, a majority of patients do not spend time speculating on whether “more better” is in reach. Instead, they normalize the new better, accept it as the current achievement, and often are content to feel stable with this level of improvement.
So far so good as long as the person discerns the improvement, because as noted above anyone who uses PAP and experiences a decrease in awakenings (insomnia) or in sleepiness (enhanced sleep quality) is highly likely to stay focused and motivated to continue PAP. In other words, these folks have an apparent potential to turn into superstar users and certainly do not resemble the quitter pathway. Some of them may turn into strugglers, the middle ground, but again if the benefits are tangible and consistent, they will continue to seek to reap the gain of PAP.
Now, here’s a crucial question that must be answered to really appreciate how clinical care fails so many patients and at the same time why insurance companies understand better than most the pitfalls of PAP therapy. “When should someone be able to declare they are sleeping better with PAP?” This question is not a hypothetical, because as noted above, a fair proportion of cases are not only not sleeping better with the early use of PAP, they are instead sleeping worse. To reiterate, it is no surprise such an individual would become a quitter in a matter of days. What we have learned at our center is the highest probability for greater use resides among those patients who declare they slept better either the first night of using PAP therapy or the first night of using a different mode of PAP therapy when they were switched from CPAP to BPAP, ABPAP, or ASV as the most common examples.
When someone wakes up in the morning from these experiences and actually notices sleep was more refreshing, quality was better, sleep was deeper and there is a sense of feeling rested, this individual has tasted and thus lived through the experience of objectively better sleep that has translated into subjectively better sleep. In a nutshell, the patient’s consciousness has been transformed overnight, because there is no way they could foresee or imagine the feelings of this changed experience.
Such individuals can always presume intellectually they expected to sleep better with PAP because it’s what they’ve heard from family, friends and providers beforehand. But to test drive PAP and to experience this change in one single night has a dramatic impact on the patient’s experiential knowledge, which will drive the person to maintain the involvement night after night, that is, start using and maintaining regular use of PAP. For this reason alone, we have long pointed out the serious problem of making patients wait 2 to 4 weeks after a titration to get their PAP devices. PAP devices should be waiting for them in the morning after the titration as they walk out the door in a model of care resembling something akin to a Bed and Breakfast, where breakfast is a new PAP setup.
We’ve already published papers describing the use of this single parameter “sleeping better” to predict who will and who won’t end up as a PAP user. And, we believe there is so much common sense to this approach, we remain continuously puzzled by the lack of attention this paradigm receives in most circles of clinical sleep medicine care, particularly among sleep medicine specialists. Most likely, far fewer sleep technologists are constrained in this way because they observe first-hand their patients’ high degree of satisfaction upon awakening from better sleep.
Tacitly, the insurance companies understand this point even though they do not put much effort into its realization. They know that if the patient isn’t doing well early on, they won’t become a regular user. We are in effect saying the same thing, but the difference is huge when considering how we attack the problem before the first titration, during the first titration and soon after the first titration. This after-care issue is crucial among those who don’t report sleeping better.
When someone says they slept worst or there was no change in sleep, we then explore the degree of motivation they are expressing. Surprisingly or not, there are a number of types of patients who write off the first bad night as a forgettable and a non-decisive factor. They want PAP, and they want it now, because they figured out beforehand it’s going to be well worth the discomfort, pain, or suffering to make it all work. These patients might suffer from serious cardiac conditions or uncontrollable blood pressure or misdiagnosed depression and so on. They are sick and tired of being sick and tired and possess enough knowledge to embrace PAP as the answer to which there is no further questions.
But, a sizeable group of non-responders (worse sleep or no change) need rapid and aggressive intervention. Some of these patients must return for a PAP-NAP. Others need retitrations within days or weeks after the first one. Some patients need a clinic appointment to ask about other options for which most soon realize PAP is the better option if there was some way to get used to it. We have worked with all these types, and we have pushed as hard as we possibly can in the most gentle and diplomatic ways among these cohorts of soon to be quitters or early strugglers.
The secret to success is the same as it is for the superstars. They have to gain an experience in which the sleeping better phenomenon hits them square between the eyes. On the most mundane level, one of the more simplistic ways to achieve this process would be to switch the patient immediately to nasal strips. Instead of haranguing them about PAP therapy, which appears impossible at the moment, conduct a rearguard action and agree with them that PAP is off the table. Then, delve into the simplicity of nasal dilator strips and inquire whether they would be willing to attempt an experiment with this intervention for a few weeks or months, after which a follow-up clinic appointment can occur.
This option is ideal because it removes all the pressure (pun intended) from using PAP. You can also start treatment with medications for leg jerks in some of these cases. In both instances, it is very common for the patient to return to clinic in a few weeks or months with a brand new perspective. They have now tasted better sleep, because of the nasal strips or the leg jerk medication. Now that they understand something physical was really mucking up their sleep and have experienced the transformation in their sleep with an easy to use therapy, all options are back on the table. Many such patients are ready to move forward with PAP as they now expect “more better” sleep to ensue.
What must we do to educate the insurance companies on the various steps in this model of care?
In clinic this week at my New Mexico sleep center, one of my sleep techs and I were discussing follow-up with a patient doing well with ABPAP therapy. He had lowered his pressures in the past year as he struggled with Aerophagia, but since starting Gabapentin for his leg jerks, he experienced far fewer episodes of air swallowing. He was very pleased with the results, and one of the main reasons for the visit was to raise his pressure settings back to higher levels. His data download confirmed some residual breathing events, mostly flow limitations and some hypopneas, and he was eager to raise pressures as well as to continue his gradual increases in the dosage of Gabapentin.
In the last portion of the appointment, insomnia symptoms were discussed. He described the classic finding of racing thoughts or “I can’t turn off my mind.” When I hear these complaints, I often query the patient on the content driving the mental wheels to keep turning. As you would imagine something deeply personal and conflictual generates the most intense emotional distress and therefore results in the greatest difficulties in setting the mind at ease. In these situations, we often see quite clearly a patient in need of psychotherapy, counseling, or perhaps a 12-step program to work directly on a daily basis on the interpersonal nature of the problems.
Occasionally, someone will mention that political news keeps him or her up at night, and the fellow we spoke to last week was one such case. No doubt, politics is a very passionate area of human behavior and conversation, which generates strong emotional reactions. Never have these points been so true than in the current political climate fueled by instantaneous media interactions, be it through internet browsing or social media entanglements. It is not necessarily that everyone has such strong views on politics in the USA, especially since data reveals as many as half of eligible voters never vote. However, it appears the expressiveness of many of those who do vote is becoming the modern rage.
In this case, unfortunately, I’m not using the word “rage” in its antiquated meaning of fad or custom. I’m referring to its baser meaning where so many people are willing to vent their hostilities when things are not going well for their preferred political agenda. Nowadays, you can tap into this rage whether you lean toward the left or right, or even if you fall along other political spectrum’s such as greens or anarchists. And, because so much can be written pro or con about any and all these political belief systems, once you go down a path to follow politics closely, your emotions are almost certain to be aroused and bound up in the drama.
When discussing this problem with our insomnia patient, one of the funniest aspects was his immediate recognition of the cause after which he commented, “My mother told me to stop watching the news before bedtime, but I wouldn’t listen.” Turns out his mother had developed the same insomnia problem and promptly solved it by no longer watching any newscasts or reading any news before bedtime.
Now, this individual was not identifying himself as an activist, which of course is a very different animal. Someone who perceives himself or herself as deeply involved in politics has good reason to live and breathe all the political information he or she can consume. The intention to use the information for action coupled with whatever emotions and reasons driving the individual toward activism would further fuel a desire to consume as much knowledge as possible. The knowledge might be about one point of view (gun control) or the opposing point of view (2nd amendment rights) with the expectation of applying this information in activist duties. We’ll return to activism in a moment.
Our patient was not an activist. He was simply caught up in the modern entanglements of browsing the web or watching too much news. He didn’t even want to discuss his political views with us, but he did recognize the behavior was gnawing at him and grinding his mental wheels to such an extent before bedtime, he could no longer fall asleep at his usual time of 11 PM. It often required two more hours to wind down again, which led to a falling asleep at 1 AM. And, he was actually losing sleep, because he still needed to wake up for work no later than 7 AM.
Our intervention was simple, because the patient not only already knew the correct solution, but also his own mother had informed him of the “treatment” several months earlier after she had made herself sick watching the news every night. She had simply stopped her focus on news after dinnertime, and therefore she stopped watching the news while lying in bed preparing for sleep. Our patient declared he was going to stop watching the news at bedtime and fully expected a relative cure of the problem. We concurred with the plan and anticipate it would succeed, albeit we reminded him that a more powerful approach is to also monitor distressing emotional experiences throughout the day so that immediate attention and coping skills can be implemented. In this way, insomniacs lessen the generation of racing thoughts at night, which are dead giveaways of “unfinished business” from earlier in the day. In contrast to the intensity and effort required to actively work through emotions throughout the day, it is nevertheless rather intriguing so many people can and have cured insomnia simply by ceasing to watch the nightly news.
Returning to activism, we are dealing with an entirely different animal where you may find many people with very decent, noble and sincere intentions, but you will also find many individuals with very serious mental health symptoms that they have learned to channel into political activism. In fact, I would venture to say, you will find an equivalent amount of mental health symptoms in the upper echelons of political candidates, leaders, strategists, consultants, and ultimately government officials.
Although I am not aware of any research that proves there is more mental health difficulties in those deeply involved in politics, it certainly seems like there is greater visibility of such symptoms. For example, regardless of which side of the political spectrum you reside on, in terms of perception most people on one side of the aisle tend to see the “other side” as filled with individuals ready, willing and able to constantly make promises that are never kept or worse, perceive the opposition is simply lying. We used to notice these traits mostly during election cycles, but now they seem almost omnipresent day in day out.
The reason this activism is such an important factor influencing insomnia is that these rounds of promises and lies make up a large proportion of what is covered in the news, and here again we have news organizations with their own slants, left and right, that seem to magnify the various lies and promises to such extremes, is it any wonder that audience passions are deeply aroused?
Thus politically-induced insomnia is probably at an all-time high and likely to stay high for years to come given how much news can be consumed on an almost minute by minute basis. When I was growing up, the news was a morning paper, evening national newscast and the local night time newscast unless you chose to read a weekly news magazine. Just think about how dramatically different news consumption was then compared with today’s news smorgasbord. It is easy to imagine politically aroused insomnia is affecting millions of individuals, unless or until they commit to ending their attachments to the screen.
One definition of rationality might be: “Rational behavior refers to a decision-making process that is based on making choices that result in the optimal level of benefit or utility for an individual, be it monetary or non-monetary.” If we substitute the word “business” or “corporation,” we could imagine such institutions make decisions either to improve the bottom line (profit) or their public relations image (reputation) or both.
So, do health insurance companies act rationally? In certain ways they must do so, otherwise they would no longer make a profit or attract a large enough membership to maintain their profits. Therefore both profits and public relations are in play in their decision-making. But, inside the workings of these businesses, it should be obvious that select territories of operations appear more rational than others.
Take the serious example of heart disease. How likely is an insurance company to deprive access to its consumers for a reasonable, if not great level of quality of care in matters of the heart? The answer is highly unlikely. Heart disease is one of the most visible health conditions as evidenced by the emergence of the “heart hospital” concept. Moreover, it’s a life and death disease process, making it one of the most dramatic of all health conditions, which thus garners it an enormous amount of attention among individuals choosing their insurance plans. As you would expect, then, an insurance plan like Medicare would cover many aspects of heart disease, otherwise there would be a huge outcry against this government-run carrier.
Not all health conditions are viewed with the same levels of intensity or interest. In fact, health conditions are best understood economically as a zero-sum game, which means there is only so much money to go around, or said another way, there will always be winners and losers just like a group of people sitting around a poker table. Heart disease is always a winner because of what’s at stake, whereas sleep medicine is often a loser because it’s commonly unclear what’s at stake.
In the big picture, then, insurance companies must determine what’s rational in managing their coverage determinations for sleep apnea and any other sleep disorders that might require sleep tests (polysomnography). Based on my observations in a quarter century of clinical practice, my sense has been most insurance policy directives toward sleep lean closer to irrational judgments much of the time, and we will proceed to discuss this problem in depth.
Let’s start with a specific clinical care problem, one I have frequently described on this site, the issue of nocturia or trips to the bathroom at night. We know three important facts about nocturia. First, nocturia is one of the largest single factors in elderly patients falling at night, injuring themselves and then requiring expensive care in follow-up, such as repairing a fractured hip. Second, nocturia is a frequent complaint among middle-aged or elderly insomniacs, because the length of stay in the bathroom often lasts more than one to two minutes, which can bring the afflicted individual to a state of nearly full wakefulness, after which returning to sleep requires a new solution, such as sleeping pills. Third, and finally, we know OSA/UARS causes nocturia (nocturiacures), and we further know treatment of OSA/UARS markedly decreases the number of bathroom trips during the night with as many as 50% of successful PAP users describing elimination of any further awakenings from nocturia urges. Even among patients who do not completely eliminate nocturia episodes, it is quite common for them to decrease trips from 3 to 4 per night down to 1 to 2 per night, a huge drop-off.
What would a rational insurance company directive dictate based on the above knowledge? The obvious response would be to find every conceivable way to aggressively treat OSA/UARS to save money caused by the nocturia episodes that lead to falls, hips fractures, and greater use of sleeping pills.
Now, how can we determine what insurance companies are contemplating regarding this issue. Surely some person or persons in these agencies has the job of reading the most up to date scientific information. Surely, someone could do a relatively straightforward cost-benefit analysis to determine what’s in the company’s best interests. Surely, someone could look at the current mess in the field of sleep medicine where so many people drop out of CPAP treatment. In sum, it would be so obvious and easy to gather all this information and come to a rational decision on what to do next.
What would the rational decision be? Undoubtedly, it would be a targeted set of solutions to increase use of a PAP machine so that more patients attained their compliant status, which based on the suppositions described above would lead to less falls, hip fractures and use of sleeping pills, all three of which cost the insurance company more money.
Yet, we know for certain that none of these steps are currently pushed by insurance companies to promote greater PAP use in their patients. In fact, the opposite or reverse stance is taken. The predominant theme of an insurance company as best we are all able to discern is that on a daily basis they focus on ways for patients to perceive a threat of losing the CPAP machine if it is not used.
Pause and ask yourself what might the intentions be of an insurer who holds an ax over the patient’s head versus an insurer offering incentives to motivate use of PAP therapy? I don’t think it’s a stretch to presume the intention is “sh*t or get off the pot.” Thus, the bean counters at insurance companies are playing with a timetable measured in weeks or months. They are imagining they will achieve user status quickly and gain whatever benefits they can derive from this cohort; whereas, the difficult cases are going to prove too costly, because the insurer might keeping paying to cover the costs of the devices, but no benefits accrue as these folks just can’t get on board to maintain use.
What’s wrong with this thinking? Why is it financially unsound? And, how can we prove that it reflects an irrational cost-benefit analysis.
To answer these questions, let’s go back to nocturia and expand on a larger subset of conditions and symptoms to show how to properly drive the analysis of costs and benefits related to treated or untreated OSA/UARS.
To begin, let’s consider all the most obvious conditions currently recognized at least by sleep medicine specialists as directly linked to untreated or poorly treated sleep-disordered breathing:
• Poorly controlled blood pressure
• Poorly controlled congestive heart failure
• Increased risks for myocardial heart disease
• Increased risks for cardiac arrhythmias.
• Increased risk of cerebrovascular accidents (strokes)
• Frequent bouts of insomnia leading to daytime fatigue and sleepiness
• Sleepiness-related car accidents and workplace accidents
• Fatigue and sleepiness related loss of productivity
• Chronic immune dysfunction of nasal and oral airways, resulting in chronic rhinosinusitis
• Aggravation of chronic depression
• Long-term cognitive decline due to chronic sleep fragmentation
• And, we’ll round out this dirty dozen with an overall sharp and steady decline in the quality of life in a person who simply can no longer muster the energy to engage in a host of daily routines that lead to a satisfying and health lifestyle.
When you think about this list, it should be readily apparent we are talking about a bunch of extremely common conditions, and you probably know some friends and family members who are suffering from these problems. This information would be called anecdotal evidence, because you probably know of some individuals who have benefited from using PAP therapy and by doing so, their blood pressure was lowered, or their arrhythmias eliminated or their productivity suddenly picked up, not to mention all the other changes for the additional conditions listed. These stories are compelling and would encourage you as well as most of us to try to persuade insurance carriers to be more supportive of OSA/UARS patients to engage them to regularly use PAP therapy.
However, the best way to gather evidence typically involves actuarial statistics, where the statistician goes through each item on the list above to determine how much money an insurance company saves by not paying for a PAP device the patient was not using versus how much money the insurer loses by the patient not using the device and suffering worse health outcomes? Another version of these data would be how much future healthcare costs are lowered by a patient using the device compared to the costs of engaging the patient to use the device?
Here’s how the first aspects of the math might look like if we scrutinized our original example of nocturia:
“ In 2013, 2.5 million nonfatal falls among older adults were treated in emergency departments and more than 734,000 of these patients required hospitalization. In 2012, the direct medical costs of falls in the United States were $30 billion when adjusted for inflation.” (1) “Published reports have suggested urgency, frequency, nocturia, and urinary incontinence are associated with an increased likelihood of falls in older adults. The inference is that these symptoms may force unexpected alterations of daily physical routines…, such as arising several times a night to urinate. Thus, urinary symptoms may be a potential target for preventive interventions to reduce fall risk in community-dwelling men and women.” (1) “In older adults, nocturia is the norm rather than the exception. Studies done between 1990 and 2009 found 68.9% to 93% of men age 70 and older get up at least once a night to void. The prevalence in women is somewhat lower, at 74.1% to 77.1%. (2) Clinically significant nocturia [2 or more times per night] is present in a majority of the elderly: more than 60% of both men and women.”(2)
In both of the articles cited above as well as a recent mission statement commentary from the CDC, (3) there are multiple references to trips to the bathroom as a major cause of falls in the elderly and yet not a single reference to the impact of sleep apnea on trips to the bathroom.
I presume you see where we’re headed. We know from other actuarial data that when an elderly person falls and fractures a hip, the costs involved in hospitalization, surgery, and recovery could amount to as low as $30,000 to a high of $60,000. So, if we take the average and stick with $45,000, the statistical question would be how many of these falls occur in a population of elderly patients with or without underlying and undiagnosed problem of OSA? Since we already know that the proportion of elderly patients suffering nocturia is extremely high, the next question would be whether or not we know the percentage of elderly patients with undiagnosed sleep apnea? Although this number is also likely to be high, we can only guesstimate, because such research is surprisingly limited.
In the course of thorough investigations, eventually someone working at a health insurance agency, a government institution like the CDC, or a sleep researcher would be able to piece together all the parts to this puzzle and make various declarations that might go something like the following bullet points:
• For each case of nocturia-related falls and subsequent hip fractures, it appears that XX% (XX% because we don’t know yet) are related to patients with previously undiagnosed sleep apnea.
• As research shows more trips to the bathroom increase the risk of falls, and that the 2nd or 3rd trips to the bathroom have a much higher risk than the 1st trip to the bathroom, it would appear that effective treatment of OSA could reduce nocturia and thus decrease falls and hip fractures.
• The cost to treat the OSA manifesting in every patient over 70 years of age turns out to range between $2,000 and $10,000 in the first year of treatment, depending upon the approach to care and the type of PAP mode prescribed as well as how effectively the sleep center and DME work together to maximize the patient’s response to PAP therapy .
• Thus, if you use the top amount of $10,000 per patient, it would cost insurers $900,000 to treat 90 patients for OSA. As each fall and hip fracture averages $45,000, you would need to prove you could prevent more than 20 falls in these 90 patients to at least break even. To be clear, 20 hip fractures would cost $900,000.
Now, the problem inherent in the above analysis is that no one suspects that the rate of falls resulting in hip fractures would be as much as 20 out of 90 patients, although no one at this point probably knows whether the number is 1 of 90 or 19 of 90. Moreover, there are numerous other variables that must be taken into account: how much do you need to decrease nocturia to see a change in the proportion of falls; to what extent will successful treatment of OSA yield the right amount of decrease to yield the results we are hoping for; and, what if elderly patients cannot obtain good care at sleep centers, because there is a bias that they cannot use PAP and a further bias that their nocturia is just an aging process?
Notwithstanding all the above, it’s clear we probably can’t come out and directly proclaim all these great savings with nocturia; however, remember nocturia is just one of the symptoms or conditions in our sample in the above list. The same analysis needs to be done to examine the prevention of damaging downstream effects for motor vehicle accidents, heart attacks, and uncontrolled hypertension and strokes and so on. Now, when you sum up the data on all these possible health incidents, then you would have a much clearer picture to what extent the insurance company is losing out by not aggressively pushing for PAP use in its members, or whether it is better off ignoring the problem, because the cost differential is not so great.
Coming up we’ll look at a few insurer approaches that mostly seem counter-productive to encourage PAP use in their patients.
- Med Reviews
- MD Edge
- CBS News
One of the most problematic and regrettable perspectives today in healthcare is the overall neglect or mismanagement of sleep complaints and related sleep disorders among mental health patients suffering suicidal ideation and behaviors. Not only are sleep disorders routinely ignored in these dire circumstances, but worse they are routinely misdiagnosed, under-treated or incorrectly treated. At the sleep conference, several of these points were highlighted, both during presentations of data about suicidal patients and by the failure to provide more penetrating analyses of the same data.
As the best example of the latter phenomenon, several poster presentations as well as lectures given at the symposium consistently described biased recruitment strategies to exclude OSA/UARS patients from protocols examining insomnia or suicidal behavior or both. You might be puzzled on the rationale to exclude sleep-disordered breathing patients, especially if you imagine as I do that SDB is a regularly occurring feature of patients suffering from suicidal ideation and behavior. Why then exclude these patients?
To understand this research approach, we need to delve a bit deeply into the topic of research design wherein researchers in general attempt to narrow the focus on the patients they study, that is, by limiting specific characteristics of the patients under investigation. For example, if you want to understand how insomnia operates in depression, you would pick a sample of patients with insomnia and depression, but you would avoid patients who also reported serious heart disease or chronic pain disorders. These two conditions could have so much influence on insomnia or depression such that you would not know at the end of the study whether or not they affected your results.
As a related example, if you were studying cognitive-behavioral therapy for insomnia (CBT-I) in depressed insomniacs, conceivably heart disease or pain conditions would affect how well or how poorly some patients responded. Of course, you could also choose to study CBT-I in a group of rheumatoid arthritis patients (chronic pain) who reported both insomnia and depression. Such a study would be valuable, but it would narrowly apply to RA patients with depression and how their insomnia responds to CBT-I.
With regards to OSA/UARS, in any of the above examples had you not excluded patients with sleep breathing problems, you would then need to account for this additional sleep disruption factor. Because the patho-physiological effects of sleep-disordered breathing lead to chronic sleep fragmentation, it would then appear to make perfect sense to choose patients without OSA/UARS. Otherwise, you might not know how to interpret the results of your study since either insomnia or SDB could be causing the sleep fragmentation.
Most researchers think in these ways to increase precision and thus keep their eyes on just a few elements. For example, to reiterate, to investigate the precise connections between depression and insomnia, you would prefer to select patients who reported just these two conditions and not much of anything else, assuming you could find such people. You would probably choose to exclude cardiac patients or chronic pain patients or those with poorly treated respiratory conditions like asthma and COPD. And, you would exclude people who had recently suffered the loss of a loved one. You can see how the list of exclusions might be never-ending. Yet, while there are many variables you would try to exclude to maintain your narrow focus, you probably would need to permit depressed patients currently using medications or those previously attempting to treat their depression. These variables are common characteristics among cohorts of depressed patients, so you might lose too many of them for your study if such recruitment criteria were too narrow.
In sum, if you include patients with too many characteristics reflecting too many different disease conditions, your treatment might not work as you expected or if it did work, you might not be so certain as to why. What if a pain patient in your research is using opiate medication for pain? Sometimes opiates improve insomnia. Ultimately, research is designed so the information can be translated, so to speak, into real-world clinical medicine. This process refers to a concept called generalizability, which is itself a bit confusing, so I will explain in a little more detail, which will then circle us back to why some people choose to eliminate OSA/UARS patients from their research.
Since most sleep patients actually suffer from lots of different ailments, in some ways it would seem odd to keep narrowing down the focus of the sample studied in your research. The narrower things get, the more you are losing generalizability. That is, your results would not reflect what happens in everyday life, because it would be peculiar to imagine you could find people who only suffer from depression and insomnia and not be suffering from several other conditions. On the other hand, if you do work with a narrow group of patients who report predominantly problems of depression and insomnia, then your results would show that treating insomnia with CBT-I works in depressed patients. This finding, though narrow, starts the process of generalizability, because you know at minimum CBT-I resolved insomnia in your sample of depressed patients. It’s best then to think of generalizability along a spectrum of usefulness. A narrow sample focus provides a narrower yet still valid generalizability, whereas a broader sample focus provides greater overall generalizability.
In current research studies on sleep complaints in suicidal patients, we are in the earlier phases of research development where the narrow focus paradigm predominates. Therefore, with this point in mind, it would make sense to eliminate OSA/UARS patients from the mix. But, there is a problem here, which some of you might quickly notice when you hear the elimination criteria would be an AHI > 10 or 15.
Think about it: if you wanted to eliminate all OSA/UARS patients from interfering in your study design, then why not pick the standard in the field for the past 30 or more years, namely, AHI > 5? Why pick an AHI that means you are only excluding moderate to severe OSA, but not excluding mild OSA? What would be the rationale for doing so? The obvious argument would likely be the more pronounced the sleep-disordered breathing the more pronounced the underlying sleep disruption. In other words, to examine a treatment for insomnia in suicidal patients, why include the confound of a more noticeable SDB-induced sleep fragmentation. Now, if we accept this principle, then why include any degree of sleep fragmentation caused by SDB? Why not exclude the mild cases of OSA as well? Or, is their sleep fragmentation so mild, it would not affect the study?
The answer to this riddle will not surprise you if you are a regular reader of this blog. The real reason they had to raise the level of AHI for the exclusion criteria is simple—the astronomical prevalence rate of OSA, including mild OSA, among insomnia patients. Thus, had they kept the standard AHI of 5 events/hr, they would not have been able to capture enough patients to conduct the research in the first place. In a way, this change in recruitment strategies is a “hat tip” to the small cadre of research groups around the globe who are actively studying the connections between SDB and chronic insomnia. As other types of insomnia research groups are exposed to the works of this vanguard of scientists, the traditional researchers have begun to realize they must look more closely at the OSA connections. In doing so, they are now confronted with the emerging paradigm that SDB is all too frequent to be ignored among insomniacs.
Overall, this new paradigm leaves many of these research groups in a quandary because they may not have the skill, expertise or motivation to appreciate and treat OSA or UARS in their insomnia patients. They may be “stuck” so to speak in wanting to continue to research through a narrow lens by imagining the prevalence of OSA is not so common. Of course, they can really only do so by claiming that it’s really moderate to severe SDB that’s the big deal, and then they are giving themselves permission to keep mild OSA (AHI < 15) in the mix.
Can we find further problems in these research studies should they choose to discount the role of OSA/UARS? I believe we can, and the way to understand the problem is to consider two of the main perspectives provided by researchers who study sleep and suicide. First, we have the theory of hyperarousal, which in general refers to the increase in EEG brain activity during sleep, which lessens the depth of sleep. In mental health, we also talk about hyperarousal while awake, referring to someone such as a PTSD patient who is hypervigilant, or in lay terms always on edge. The second theory refers to the sequencing or timeline in how we view the longitudinal relationship between specific sleep symptoms or disorders and the final outcomes of suicidal thinking, behavior and ultimately death. Both of these aspects overlap, so our continued discussion will attempt to weave things together.
The ultimate in hyperarousal during sleep would be a disorder that constantly fragments sleep, causing either brief or lengthy arousals from a few seconds to much longer periods of wakefulness. The ironic history on sleep fragmentation research is the out and out failure of so many investigators of insomnia to repeatedly declare that hyperarousal observed regularly in such patients has no obvious cause, other than to declare “insomnia is a hyperarousal disorder.” This statement is much less useful compared to a declaration like “cars driven through red lights spend more time in junkyards.” In both instances, something is being fractured, your sleep or your car, but the first statement (about sleep) provides no cause for the break, while for the car you can at least suspect that driving through red lights must lead to more crashes that total cars, landing them in junkyards.
Insomnia research for decades has attempted to drive home the point that the cause of sleeplessness is the sleep fragmentation due to hyperarousal, yet without providing a clear mechanism through which the brain becomes aroused. Indeed, the most common explanation is “the brain of an insomniac is hyperaroused” and probably genetically predisposed to be so. The irony of course is that OSA/UARS are leading precursors to and causes of hyperarousal. The argument is not that OSA/UARS needs to be understood as the only cause of hyperarousal among chronic insomniacs, because these individuals may also suffer from a predisposition of some sort, but the fact that so much recent research shows high rates of sleep-disordered breathing among insomniacs should be raising a very large red flag about the incomplete state of affairs observed in most insomnia research.
If OSA/UARS are major contributing or causal influences on the excessive arousal activity in the brains of chronic insomniacs, and treatment of these conditions leads to clear-cut decreases in hyperarousal, aren’t we obligated to wonder just how much SDB is operating in these patients? Why continue to espouse the belief that hyperarousal is simply innate to insomnia when you can easily observe and document (with the correct respiratory sensors in the hands of a competent sleep technologist, interpreted by a competent sleep specialist) this connection between SDB and EEG arousal? Again, as described in earlier posts, we are moving closer and closer into the realms of potential medical malpractice. It is not reasonable to keep prescribing hypnotic medications to insomnia patients to tamp down their hyperarousal for more than a decade without ever considering the possibility the hyperarousal has a cause other than genetics. It is a requirement of standard of care paradigms to ask the question: why don’t these drugs work or why don’t they work very well? Moreover, it is an ethical requirement of a physician or a prescribing psychologist to be curious enough to wonder if something is being missed in the differential diagnosis (the list of conditions or diseases we suspect might be causing the problem at hand).
Perhaps the greatest barrier to accurate and timely recognition of the presence of OSA/UARS in a suicidal patient with sleep complaints is the nearly ubiquitous example where these patients present with symptoms of insomnia or nightmares or both. Because insomnia and nightmares are so vexing to the patient and often described with desperation and other emotional distress, it would be surprising for a psychologist and even a sleep physician to not be swayed into thinking that insomnia and nightmares are the primary sleep conditions to be evaluated, diagnosed and treated. Unfortunately, what we have seen for more than two decades is that either or both insomnia or nightmares are more often than not a flare in the sky signaling the presence of a sleep breathing disorder as a potentially much larger threat to mental and physical health. This sleep breathing disorder resides, figuratively, in a place hidden from the eyes of the patient and the provider, thus leading to its relative invisibility and delayed identification unless someone interprets more comprehensively the meaning of the flare above.
Still another confound is the link between insomnia and hyperarousal as well as nightmares and hyperarousal. Both links have been written about for decades and have led researchers and clinicians to reasonably make the assumption nightmares and insomnia are the source of excessive arousal activity. Our point is nightmares or insomnia could also be considered downstream effects. Evidence for this perspective is mounting, because research continues to show OSA/UARS treatment decreases both insomnia and nightmares. In this paradigm, we would then look at the sleep breathing disorder as the source of the hyperarousal activity, which somehow caused insomnia and nightmares or somehow catalyzed a part of the brain’s systems to increase vulnerability to develop the problems of insomnia and nightmares. Either way, the net effect is logical: if SDB treatment decreases insomnia and nightmares along with their related hyperarousal activity, then we would no longer link the hyperarousal directly to these usual suspects despite their being the more obvious sleep disorders in plain sight. Instead, we would need to declare the primary culprit as sleep-disordered breathing, the ultimate upstream activity that all along the way was leading to hyperarousal.
However, we could also trace things further back in the sequence to investigate the brain itself and ask the question of whether or not something in the brain of the suicidal patient adversely alters the way the person breathes night or day and whether such a finding could lead to the eventual development of OSA/UARS. In some ways, this theory is even more appealing, because there is no apparent logic that supports the idea most suicidal patients with insomnia and nightmares should have sleep-disordered breathing. Whereas, if you could discover something “wrong” in the brains of suicidal patients, it would make intuitive sense to believe brain dysfunction was the ultimate starting point of the problem, that is, the ultimate upstream factor. Next, the research would need to confirm whether or not this brain problem/change/condition in fact can be shown to alter nocturnal respiration and lead to sleep-disordered breathing.
In looking back over this post (multiple times) I can see how it feels circuitous. Though not necessarily intended, I wish to point out that a lot of ideas in research come about through circuitous pathways. Some may imagine there is a more logical stream of ideas that neatly package themselves together in linear fashion and then proceed step by step to inevitable outcomes. As far I have observed in research, the pathways are often choppy, misdirected, and lacking any obvious destiny to a final set of definitive observations.
Again, here we are 45 years after Guilleminault and colleagues reported in 1973 the first cases of insomnia linked to sleep apnea. And, yet in the present research environment that investigates conditions such as we have been discussing suicidal ideation and behavior and completed suicide there remains tremendous resistance if not outright ignorance on the rather obvious problem of chronic sleep fragmentation induced by OSA/UARS in these fragile patients. Instead, these deeply suffering individuals are repeatedly informed the problem is in their minds, their neurotransmitters, their genetic predisposition, or perhaps their sensitivity to environmental or psychological stressors, without ever once hearing about the possibility that their rotten, degraded, no-good sleep is the perfect substrate that feeds the fire for all these other contributors to their disheartening and demoralizing anti-life perspective and attitudes.
It cannot go without saying what a dramatic turn of events may arise AFTER A GOOD NIGHT’S SLEEP!
Yet this pearl of wisdom continues to be relegated to a footnote in the patient’s care, if that, due to all the biases described above. Where does that leave us in our efforts to help these patients?
Not in a very good place in my estimation as both clinicians and researchers demonstrate only a fair degree of motivation to want to engage this way with their patients or samples of patients for studies. This silo effect has been repeatedly described and has proven pervasive in numerous fields of medicine, wherein a subspecialty of any type can develop its own brand of tunnel vision, after which new information is nearly impossible to disseminate within the confines of the subspecialty itself.
Imagine right now that every family member with a suicidal patient read this blog and then proceeded to contact a primary healthcare provider, mental health or medical, demanding their loved one undergo sleep testing. Sadly, far greater than 50% of the doctors or therapists would imagine only that the family member was grasping at straws and the other smaller half might imagine the idea was interesting but would have no conceivable way to take action; or, they would believe there was nothing they could do about this new information.
So, again what would happen? The answer is nothing in most cases. This last point highlights the frustration of so many patients and their family members who ultimately must confront these narrow perspectives so routinely expressed by many healthcare professionals. Internet access and unlimited availability to growing knowledge bases will have some impact on these processes and may speed up the translation of scientific evidence into actual clinical practice.
In the meantime, many individuals continue to suffer and continue to engage in suicidal ideation and behavior, and some successfully kill themselves. Yet, there is no way to declare that had the true nature of their sleep disorders been correctly diagnosed, they somehow would have been spared these tragic endings. There is a great deal of complexity to suicidal behaviors and suicide, so the jury is out on the extent to which sleep fragmentation triggered by undetected OSA/UARS aggravates these mental health problems. Nonetheless, we already know that treating insomnia and nightmares, each one independently, appears to decrease suicidal ideation and behavior. Therefore, it certainly seems reasonable to hypothesize that OSA/UARS is an active component of these processes and merits much greater attention in research circles.
With the above in mind, here’s my modest proposal. Let’s collect the top 100 mental health researchers of suicide in the world along with the top 100 government grant administrators or related officials who oversee the distribution of funding for suicide research. Next we place them in various sleep laboratories around the globe, hook them up to EEG monitors and then proceed to keep them awake for days on end. At most, there are permitted to experience two hours of sleep, but overall whenever they sleep it must be highly fragmented through the use of artificial techniques, such subtle sound waves to kick them out of deep sleep. Then, over the course of days we would observe their psychological status and video tape their rapid decline in mood, culminating in some instances in depression and suicidal ideation and possibly self-harming behaviors. Finally, we would ask each of these research subjects when he or she would like to be permitted to sleep normally again, which would be affirmed by all of the individuals sooner or later.
Once they recovered from their sleep fragmentation/deprivation, they would be asked to watch the videos of their behavior. Then, they would be asked whether or not they have a new perspective on the value of healthy restorative slumber? Finally, they would be shown the videotape sections where they began to demonstrate suicidal ideation or behavior, as applicable. Afterwards, they would go through a series of didactics to learn about the role of sleep-disordered breathing and how it causes the sleep fragmentation/deprivation they had been exposed to in extreme fashion to mimic what suicidal patients might be experiencing chronically year after year.
Would some of these professionals get it? Would the light bulb go off in their heads? Again, sadly, probably not a lot, but for sure some what finally understand. Indeed, a lot occurs when any individual actually experiences the problem of SDB first hand. That alone would be enough to “wake up” the individual from the slumber that had prevented him or her from understanding how badly poor sleep had affected mental health and mood.
Though the experiment above might be a game-changer, we’re more likely to see the change through the methodical development of research studies proving these points. On an individual basis we might see some new trends emerge soon. But overall, unfortunately, I must say I won’t be holding my breath regarding rapid changes in policies and guidelines to help suicidal patients.
Sourced from Classic Sleep Care – Sleep & Psychiatry Symposium – A recap of detailed lectures
One of the most interesting sessions I attended in Baltimore delved into the impact of sleep disorders in mental health patients. As I’ve repeated, ad nauseum, how we specialize in mental health patients with sleep disorders, this topic naturally piqued my curiosity, and it did not disappoint.
Three main speakers covered specific topics often including case report information, and a fourth served as a discussant; this final speaker also brought up hypothetical cases to review to integrate the material from the earlier speakers.
The three speakers gave very thoughtful and detailed lectures, all of which pointed to the imperative to closely examine the nature of the sleep disorders in various psychiatric patients. The first presentation was entitled, “Common Psychiatric Conditions in Adults who Present with Sleep Problems.” This talk presented by Dr. Sam Fleishman set the table by clarifying the need to realize that sleep symptoms—all manner of sleep symptoms—can often be manifestations of underlying sleep disorders. He focused on insomnia, sleep apnea, restless legs, leg jerks, and circadian rhythm conditions.
Among the many important insights offered in his talk, three stood out for me. First, there is a growing recognition that circadian rhythm abnormalities may not just be associated with mental health problems, but also these schedule irregularities may be causing or aggravating these conditions. Second, the hopelessness that often arises from chronic insomnia may itself be a risk factor or otherwise contributes to suicidal ideation. Third, more attention needs to be given to residual insomnia especially in the context of failed antidepressant therapy when treating depressed patients with sleep complaints. In other words, is insomnia a co-morbid condition or still something secondary to depression? The verdict seems clear on the co-morbidity angle, but it remains uncertain how many practitioners in mental health fields recognize this distinction and how much it impacts therapeutic decision-making.
The second talk, by Dr. Ann Ivanenko, entitled “Common Psychiatric Conditions in Children and Adolescents who Present with Sleep Problems” made key points for these age groups that aligned with the first talk on adults. In addition, there is increasing recognition of the prevalence of other sleep disorders in patients with ADD/ADHD such as RLS/PLMD and sleep-disordered breathing. There was a brief mention of the problem of racing thoughts in children as a classic manifestation of insomnia, but I was expecting some commentary on assessment of enlarged tonsils in this age group, because such patients often suffer OSA/UARS. If you were not aware, many children report a decrease in racing thoughts following the T & A procedure.
The third talk, “The Impact of Psychological Issues in Parents on Management of Sleep Problems in Infants and Mothers” was presented by Dr. Reut Gruber, but unfortunately I was called out of the workshop to deal with a sleep center problem back in NM. As you can imagine, this talk would have covered the gross sleep deprivation experiences parents must struggle with when attempting to resolve insomnia and other sleep disorders in their young children.
Last, Dr. Merrill Wise, presented as a Discussant in his talk, “Navigating Through Sleep Clinic When It Seems Like Psychiatry Clinic” and spent most of his time on interesting patient case histories to highlight many of the points brought up by the earlier speakers. In so doing, he delved into an adolescent case of delayed sleep phase syndrome and an adult case where the patient had difficulties adapting to PAP therapy. In the former case, he discussed how something as simple as bright light therapy, timed for effective intervention, might be a valuable tool to employ in adolescents who commonly report this delayed schedule problem. In the adult case, he pointed to many of the behavioral interventions, such as mask habituation strategies (e.g. learning to wear it in front of a TV to overcome and distract from its sensations), and cognitive-behavioral therapy for insomnia wherein the PAP user may have to abide by the strategy to not try to go to sleep with PAP when not sleepy. In sum, the points were made repeatedly in this last talk as well as throughout the symposium that just because a sleep patient looks more like a mental health patient, we still owe it to these individuals to aggressively treat their sleep problems, often as co-morbid conditions, with a reasonable expectation their mental health symptoms will decrease in severity.
I concurred with virtually all the points made at the symposium and expressed my gratitude for the fine talks and discussion between the members of the panel. However, I expressed a need to consider making these points in a stronger and more assertive fashion. In particular, I brought up several points in the Q & A discussion afterwards, and later reiterated several facets of how we operate our sleep center in the management of mental health patients with sleep disorders. In this blog post, I will now elaborate in more detail on the various “bullet points” I offered at the end of the symposium, and my hope is that more mental health providers and sleep medicine professionals will heed this call for more aggressive strategies in dealing with sleep problems in psychiatric patients.
Here are the bullet points, after which I will elaborate:
- Spotting the sub-optimal responses to psychiatric treatment is a huge red flag for undetected sleep disorders.
- Ironically, the psychiatric community is currently blessed with its own diagnostic manual, the DSM-V, in which resides a compendium on sleep disorders, the likes of which puts many professional sleep publications to shame.
- The co-morbidity angle is where it’s at and should always be at the top of the list of the differential diagnosis in sorting out sleep complaints in mental health patients.
- Signs and symptoms of nonrestorative sleep may prove to be an even larger signal telegraphing the necessity to suspect undetected sleep disorders in patients with psychiatric disorders.
- Contrary to the conventional wisdom, and no surprise to readers of this blog, CPAP is not only a poor starting therapy for OSA in psychiatric patients, but also CPAP itself often proves to be a traumatizing stimuli that disrupts and delays actual use of PAP therapy for months or years.
- Last, using advanced PAP therapy modes (ABPAP, ASV) as well as repeat trips to the sleep lab for desensitization experiences (PAP-NAP) or retitrations (REPAP) are the foundational keys to enhancing adaptation and increasing hours of use (along with adherence) in challenging mental health patients with OSA or UARS.
Sub-optimal responses. This construct, or more simply, the way in which patients report less than stellar results to their treatment will one day be viewed as the most glaring error made by the professional psychiatry and psychology communities, because it prevented them from recognizing how frequent and how much these undetected and untreated sleep disorders were ravaging the mental health of their patients.
Throughout all of medicine, a sub-optimal response almost invariably triggers further exploration of additional contributing factors to someone’s poor health. When a diabetic is not responding to medications, we evaluate the timing and dosage of meds. If the meds check out, we go back to the basics of diet and exercise. When things are persistently subpar, we look for other contributing factors such as whether the diabetes represents a more complex problem, needing not just one or two medications, but maybe 3 medications and possibly insulin. And, in some cases, it becomes imperative for an obese patient to commit to losing at least 10% of their excess weight.
This same phenomenon occurs in a much more narrowed scheme among numerous psychiatric patients, particularly those suffering from depression. There may be a discussion of adding psychotherapy, prescribing regular exercise, and of course adjusting and revising medications. But, dealing with the sleep disturbances falls to the bottom of the list of things to reevaluate or newly explore. Yet, the sub-optimal results routinely look just like an undiagnosed and untreated case of insomnia or OSA/UARS or both. The patient says the depression is somewhat better, but they still feel tired or fatigued throughout the day. Sleep is a little better, but there are still far too many awakenings during the night and not much pep in the morning upon awakening. Small or not so small clues also could be noted if the patient reports persistent nocturia, a symptom rarely discussed between psychiatric patients and their mental health providers. Another issue would be hypertension creeping up slightly or concerns about cardiac arrhythmias. These two symptoms could easily be explained away by a psychiatrist or psychologist as stress-related, if they do not know how these common medical conditions connect to OSA/UARS. To repeat, the report of a sub-optimal response to psychiatric treatment should be an automatic, “do not pass GO, do not collect $200…go straight to the sleep center!”
DSM-V Sleep Disorders Section. The fields of psychiatry and psychology are now very fortunate because their main guiding manual for diagnosing patients was re-written just a few years back to focus on the critical importance of looking at sleep disorders as independent conditions affecting psychiatric disorders instead of the older and conventional way of relegating the sleep disturbance to secondary status as if the mental disorder was the sole cause of the sleep complaint. This traditional view has been extremely problematic because it meant and still proposes that the vast majority of mental health patients must traverse tortuous pathways to eventually have a healthcare provider of assorted stripes recognize an ongoing and undetected independent sleep disorder is playing a much larger role in the clinical picture. Sadly, most mental health providers continue to misdiagnose their patients in this way, that is focus on the mental issues and avoid the sleep complaints. Yet, now they have this wonderfully concise and accurate section in the DSM-V. If they would read and study this material, it would advance their practice skills enormously, and it would lead to much more accurate and timely diagnoses of sleep disorders in their patients.
Concepts of Co-Morbidity. This issue reprises the one above by seeking to eliminate the old terminology of “sleep disturbances due to a mental illness,” which had been in use for arguably a century or more, starting well before the use of the DSM manuals. The great value that arises from the use of the “co-morbidity” construct is that ultimately it will change the way both sleep and psychiatry are practiced. As I alluded to in other posts and which I discussed with several colleagues at the conference, the field of sleep medicine should prepare itself for the inexorable slicing up into various niches.
If we look just at the fields of psychiatry and psychology we can make several predictions that to my way of thinking are virtually inevitable. First, training to become a psychiatrist or psychologist is going to change sooner than later, where these professionals will likely be required to complete six to twelve months of sleep medicine training. Some might argue that we already have programs called “sleep fellowships” similar to other types of fellowships for medical subspecialties. But, I do not see such an approach maintaining itself long term for mental health providers. Because their work and training directly involves care of patients, millions of whom are actively suffering from sleep disorders, it is common sense to start training these healthcare providers in the trenches where they work, not separately in some other sleep-oriented facility.
Moreover, this problem is so widespread, we could be talking about 80 to 90% of mental health patients, because when you just glance at the DSM-V, you notice virtually every disorder listed includes a sleep disorder factor, which Dr. Lieberman noted in his talk. And, making matters more acute, psychiatric hospitals in particular will need to insert sleep testing equipment into their facilities, because so many inpatients also suffer from these undetected and untreated conditions, which most likely are delaying patients from receiving optimal care in the hospital and quite possibly prolonging their hospitalization. I would anticipate most psychiatric hospitals will need to employ a sleep specialist at their facilities, and once this process embeds itself, a short time later, all the psychiatric residents or fellows (the next levels of training after medical school) will clamor for education from the sleep specialist.
While the above will create major disruptions to current care in mental health, I believe such processes are inevitable given the obvious improvement in outcomes that will follow. Currently, just among public awareness, tons of people are describing their experiences through social media and mainstream media on how life-changing their sleep treatments have been. Chief among these treatments are PAP therapy. Therefore, the earliest disruption we will see could be family members demanding that their loved ones be permitted to bring their PAP devices with them during their psychiatric hospitalizations.
Nonrestorative sleep. This factor has also been crucial in understanding the sleep problems in psychiatric patients. The concept was brought up several times during the symposium. A singular point I brought up was the imperative to appreciate that this particular complaint almost always is sufficient to qualify a patient for a sleep study or most certainly a comprehensive sleep medicine review of symptoms and complaints.
However, my concern remains that most people linked to mental health professional facilities and institutions imagine that feelings of fatigue or daytime lethargy or not feeling rested in the morning (all three can be signs of nonrestorative sleep) are simply signs of depression or some other psychiatric co-occurring symptom or disorder. I am in no way suggesting these mental health factors would not contribute to these feelings; I am urging my colleagues to realize that sleep disorders are in the equation as well. And, for years, we have often used the single question: “is your sleep refreshing or unrefreshing?” to rapidly assess a patient’s probability for an objectively diagnosable sleep disorder. In our clinical experience, the “unrefreshing” answer is linked to diagnosable and treatable sleep disorders in well over 90% of cases. I trust mental health professionals will find the same to be true once they push to evaluate these patients with comprehensive or diagnostic sleep tools.
CPAP Traumatization. This problem remains my greatest concern of all because of the many patients who suffer from the consensus opinion that nearly anyone can adapt to CPAP if they just try hard enough. What a joke!? If more than half the patients who try CPAP are quitting in the first few weeks or months, among which are many who reject CPAP after just one night in the lab or just one night at home, I do not see how it is reasonable to make the assumption there is something “wrong” with all these patients. Logic dictates it would be just the opposite—there must be something wrong with CPAP!
There is something wrong with CPAP, and it centers around two key features of this technology. The first and most obvious is that CPAP, even auto-CPAP provides exactly the same pressure on inspiration and on expiration at any given moment in time and space. In other words, even if the CPAP is auto-adjusting, breath by breath you get the same pressure breathing in or out. You may turn on your back or enter into REM sleep, but once the CPAP device (if in auto mode) adjusts, the pressure is fixed on inhalation and exhalation. This constraining feature of CPAP sets the stage for expiratory pressure intolerance, because the human body in responding to PAP in general needs higher pressures when breathing in, but lower pressures when breathing out. Expiratory pressure intolerance occurs because it is unnatural to breathe out again such high pressures. This finding was established in 1992 in a study first demonstrating that bilevel settings were different anywhere from 2.5 to 7.5 units higher on inspiration as on expiration, and yet still established normal breathing on both limbs of respiration.
So, CPAP is wrong because the pressure is too rigidly delivered, and it’s wrong again because it cannot adjust sufficiently during expiration. Even with the use of expiratory pressure relief (EPR) systems, we do not find an adequate or consistent response, because EPR is more or less a mini-bilevel response. Thus, we move nearly all our patients onto auto-adjusting dual pressure devices, such as ABPAP and ASV.
Advanced PAP and Revisiting the Sleep Lab
On this blog, you have seen many past references to our use of advanced PAP devices and the need to return patients to the sleep lab where we can fine tune their experiences with these sophisticated technological devices. The key driver in this approach derives from auto-adjusting algorithms in the ABPAP and ASV devices, which on the one hand provide much greater sensitivity to necessary changes in the pressures for the individual (e.g. when changing sleep positions, entering REM sleep), but on the other hand are not consistently effective in managing the common residual problem of flow limitation or RERAs in the attempt to fully normalize the airflow signal.
This problem fits into the OSA equation under the general question: “How do we diagnose and how do we treat upper airway resistance syndrome (UARS)?” UARS has been a controversial diagnosis for many years, and the greatest of all ironies from our perspective is that this variant of OSA appears to be especially common in mental health patients. A further barrier to care in treating UARS is that it almost always requires higher pressure settings to attain a fully normalized airflow signal. In other words, mental health patients often need much higher pressure than might other patients with less UARS activity in their sleep breathing disorder, yet because of the nearly ubiquitous problem of anxiety among psychiatric patients, we often observe they cannot tolerate the higher pressures.
If you look at the two slides below, you can understand the general nature of this problem. When you suffer from a fully collapsed airway, an apnea, it takes very little pressurized air to re-open your airway, if just a little bit. This treatment is not like inflating a balloon, where you need lots of pressure in the very beginning to start inflating. Just a little pressure converts the apnea to a hypopnea. Then, adding just a little more air pressure converts the hypopnea to the flow limitation event. Finally, the highest pressures are needed to bring the airway fully open. The pictures with my hands are offered as a figurative example of how the airway transitions from apnea to hypopnea to flow limitation and finally fully open and normal airway.
This understanding of the treatment of OSA/UARS with PAP led us nearly a decade ago to use these devices in mental health patients and with that our publication of several research papers describing these processes and their advantages over CPAP in this patient population.
Sourced from Classic Sleep Care – Sleep & Psychiatry Symposium – A recap of detailed lectures