Sleep Apnea Patient Centered Outcomes Network (SAPCON): Part 5

Last year, Sleep Review Magazine published an introductory story about the SAPCON project, which focuses on collecting input from patients with sleep apnea as a way to “democratize” research and gain valuable insights to promote more effective treatments. Sleep Review published a follow-up story to discuss the preliminary findings, which you can read about here on pages 26-28. 

This article is the fifth in a series, following:

Part 1 – They said I need a machine, that’s it?
Part 2 – So I have sleep apnea? So what?
Part 3 – Are there options besides CPAP?
Part 4 – Frustration rapidly leads to non-adherence

Fifth Challenge: Delays in diagnosis or outright misdiagnosis.

In this section of the study, the authors focus on the long-standing problem of diagnostic delays, which, for some patients, may be up to a decade or more. In particular, females and ethnic minorities demonstrated disproportionately low rates of referrals and thus diagnoses. The authors infer the crucial point regarding so many of these undiagnosed individuals: the development of cognitive impairment leads to executive dysfunction. In other words, these individuals may have greater difficulties in understanding the nature of their problem and become frustrated in their efforts to overcome it. We refer to this process as “the disease protects itself”, through which OSA damages the mind in various ways, the individual struggles to effect the best treatment options, and in many instances the condition defeats the therapy.

Another noted problem is the variability in sleep apnea phenotypes, meaning the signs and symptoms that patients describe to referring doctors, which then trigger a referral to a sleep center. This issue remains especially problematic, because so many primary care physicians still believe snoring and sleepiness are necessary symptoms to qualify for a sleep test.

In the last segment of their discussion, a quote from a patient regarding what presumably refers to expiratory pressure intolerance stated: “I can’t keep the mask on all night, it feels like it’s breathing against me, so it goes off.” And then a follow-up quote with a similar patient, speaking to the approach we use regularly among our second opinion patients: “One sleep doc told me I wasn’t giving it enough time. I’d struggled on PAP for years. Finally, a second opinion showed I had complex sleep apnea. My new [advanced PAP] treatment is making a massive difference.” This last example refers to a patient having waited years to ultimately receive the correct diagnosis, complex sleep apnea, which is the condition where standard PAP, usually CPAP but also from APAP or BPAP, triggers the side-effect of central apneas, thus requiring the use of more advanced technology. 

These two points, delay in diagnosis, which is really delay in patient referral, and misdiagnosis are banes on the field of sleep medicine. Regarding the former, one would think the epidemic of sleep apnea would finally bring some urgency into the world of primary care. The pace of referrals in the various sleep systems may be increasing but nowhere near the capacity of what could be provided if all sleep centers were maxed out. Unfortunately, there is little to be done on this issue other than long-term strategies, because patients frequently do not take sleep issues seriously nor do their doctors probe for sleep disorders in an efficient and timely way.

Once someone is undergoing care in a sleep center system and attempting PAP therapy, the scope of opportunities is greatly widened to aid the individual. However, many sleep centers still do not realize how to expand their range of services.

We see numerous cases every week in which patients’ objective data downloads indicate the presence of central apneas. Many of these patients started at our center and were using either APAP, because they were directed to by an insurance carrier that denied them the opportunity for a titration in a sleep lab, or they were using ABPAP, an advanced PAP mode that provides very precise improvements in treating residual breathing events, but which also may trigger central apneas in a number of patients. Every week we are recommending to patients to return to the sleep lab for evaluation of these central apneas to determine whether an ASV device would prove more effective, presuming the patient will qualify for the diagnosis of complex sleep as described in the SAPCON authors’ example.

It should be bad enough that other sleep doctors are not picking up on this finding of residual central apneas and actively seeking to resolve the problem, but it turns out this system wide lack of responsiveness is a proverbial tip of the iceberg in the deeper problems affecting such patients. Commonly, when this issue is presented to other sleep doctors, a frequent refrain is to declare a few central apneas mean very little and should dissipate over time anyway. Interestingly, you will meet sleep physicians who marshal the same talking points when treating a CPAP user, who three years after starting still shows a small number of residual central apneas. Even if they cannot provide a rationale for the persistence of central apneas, they will fall back on “what are a few central apneas in the big picture?”

The finding of a just a few central apneas in any patient at any time is not necessarily grounds to immediately insist he or she needs ASV therapy, but the deeper problem is objective data almost unequivocally indicates a serious adaptation problem emerging, one that often does not resolve. The specific adaptation problem is the patient needs higher pressures but cannot tolerate higher pressures. Although unproven and difficult to research, our working theory describes this phenomenon as a simple mechanical response. Namely, the individual feels the pressure in the throat as a series of uncomfortable sensations, which then triggers the person to cease breathing in the same way someone feels a sort of breathing startle when sticking her head out of car window travelling at high speed.

The paradox here is the need for the higher pressures to eliminate residual breathing events (flow limitations, obstructive hypopneas, and obstructive apneas), yet the higher pressure triggers a mechanical response, leading to the iatrogenic side-effect of central apneas. Said more simply: shove too much air down someone’s throat and the brain reacts to cease breathing temporarily.

It should be clear to sleep professionals this double-bind is quite common in clinical practice, and it may be observed by more sleep docs and sleep techs than we can know, but it is not acted on in dynamic and timely fashion. And, in my experience and in my opinion of the larger field, I assume this double-edge sword is a leading and potentially the greatest single factor in preventing patients from long-term use of PAP therapy or in gaining anything close to optimal results.

This point of view when taken to its limit creates a great deal of consternation in managing patients whose health insurance systems consistently deny them the opportunity for more precise fine-tuning of pressure settings in the sleep laboratory. Although these barriers have been in place throughout the USA for several years, we are now seeing this rigid policy manifesting in more of our patients in New Mexico. And, I will mention of the last 10 patients on auto-CPAP (APAP) who have never been tested in a sleep lab for diagnostic or titration purposes, all showed objective issues on their data downloads that warrant further investigation under the microscope of the sleep lab. To date, only one of the 10 has received permission to be further evaluated in the lab.

Unquestionably, some of these patients are gaining benefits from using APAP, so it is not unreasonable the insurance carrier insists that mask issues and related leak and mouth breathing problems should be effectively managed from a cost-savings perspective by the DME company or by staff at the sleep center without the patient needing a lab retitration. We accept this perspective and work with patients through their DMEs or via our sleep techs to find solutions to these specific problems. However, when no solutions emerge as is common in 30% of OSA/UARS patients, and these same patients are manifesting residual breathing events such as flow limitations and central apneas, then the patient needs to receive a higher standard of care in the sleep lab. While all these patients are usually reporting some improvement in outcomes such as decreased sleepiness, nocturia, and insomnia, their completion of follow-up surveys for these symptoms often indicate sub-optimal results. Again, combining all this information to build a larger context on how the patient is responding to PAP should be sufficient grounds to convince the insurance carrier more advanced steps are needed for optimal management.

This larger context yields a very surprising insight, because the big picture turns out to be more than central apneas. When we try to treat flow limitation events, we objectively see in the sleep lab whether the patient tolerates higher pressures on expiration. When they struggle at this point, they show the objective finding (on the airflow tracing) called expiratory pressure intolerance or EPI. And, from our experience, we see the EPI before we see the central apneas emerging. In other words, EPI appears to be the pathway that leads to central apneas in some patients, and many individuals with OSA/UARS show EPI on CPAP, APAP, BPAP and even on ABPAP. Thus, a clinical and research question should arise on what can treat this pervasive problem of EPI prior to the onset of central apneas. Yet, this problem is only researched by a few groups in the world; and, the most remarkable finding to date is that ASV despite the absence of central apneas, offers a very precise capability to aggressively treat flow limitation while preventing EPI.

This last point has been lost in all the recent concerns and confusion about prescribing ASV in heart patients with severe congestive heart failure. But, even before this cardiac issue emerged on the medical landscape, nearly all sleep doctors presumed that ASV was only relevant to patients with central apneas, based on either of two conditions: primary central sleep apnea or complex sleep apnea.

Our view is based on anecdotal evidence in which we tested individuals with ASV who previously failed CPAP, APAP, BPAP, ABPAP and any possible expiratory pressure relief system such as CFLEX or EPR. All these patients showed EPI but did not meet the requirements for complex sleep apnea. Nonetheless, they were intolerant of all other devices and desperately wanting to treat their sleep breathing disorder. At that point, we recommended a trial of ASV in the sleep lab to determine whether or not it would indeed eliminate the problem of EPI, which resulted in most cases. Afterwards, greater than 70 to 80% of these patients reporting sleeping better with ASV, and several wondered why they could not have been exposed to this PAP mode earlier in their treatment course. Finally, when we appealed to insurance carriers in some cases with explicit details of the problems, some patients received coverage for the ASV device. As a testament to ASV, others who did not receive insurance coverage elected to purchase the device out of pocket.

Wrapping up, let’s return to the second point of discussion, sleep apnea phenotypes. This issue also brings us back to the relatively unsolvable problem of dealing with medical professionals outside the field of sleep medicine. In the setting of primary care clinics, these doctors, nurse practitioners, physician’s assistants, nurses, and various other support personnel often do not organize a cohesive intake system to capture more patients with OSA/UARS. As noted above, there a huge proportion of medical personnel still believe the combo of snoring and sleepiness combo is the only way to punch a patient’s ticket to visit a sleep medical center and receive diagnostic testing. As an aside, some of these doctors are now ordering their own home sleep tests (HST), and once again the same issue arises. Because they are not aware of deep connections between insomnia and OSA/UARS, these physicians are more inclined to not order the HST on the insomniac, but instead prescribe sleeping pills.

This particular phenotype problem is arguably the most frequent way for comorbid OSA/UARS to go undiagnosed among insomnia patients, but there are many more instances where the phenotypic presentation leads astray medical professionals working outside the field of sleep medicine. Some of the most common examples include patients with mental health disorders, especially depression and PTSD, chronic pain patients as well as numerous other medical conditions where the approach is to first rule out various medical disorders before raising suspicions about a serious sleep disorder as the primary culprit in the patient’s symptoms. For all of the above stated reasons, it is easy to see why some patients take up to ten years to receive the correct diagnosis.

Barry Krakow MD


Dr Krakow’s 27 years of sleep research have focused on the complex relationship between physiological and psychological sleep disorders. Dr Krakow currently operates private sleep medical center, Maimonides Sleep Arts & Sciences, Ltd., and serves as Classic SleepCare’s paid Medical Director.

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