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AHI vs ODI
#1
Hello,

I just had some questions regarding my first sleep study, and while I know that many of you are not doctors, I figured that your years of experience would have given you some insight into these things.

To begin, I initially went into the sleep study with my only symptom being excessive daytime sleepiness. I've never snored, which has been verified by a number of people, including ex's, my husband, friends, and classmates (I tend to fall asleep in a variety of social settings, so I have numerous people that have all confirmed this for me). I didn't really think I had sleep apnea, and I'm still tentative to believe the results that were given to me. I was given a wrist monitor to bring home that would monitor my blood oxygenation levels, pulse, and wake/sleep stages.

Firstly, when going over my wake/sleep stages, the woman with whom I was speaking said that certain highlighted red areas were when I was awake. I accepted this at face value because I saw several red areas and knew that I had woken up several times during the night (once to urinate, so I know that I was completely conscious and several other times I distinctly remember checking to see if my device was still on). However, going back over the results later, it is completely clear that the red marked areas are my REM sleep stages, and it doesn't show me waking up at all during the night, which I know was not the case.

Additionally, the criteria for this sleep studies' measurement of AHI was an oxygen desaturation level of greater than or equal to 3% (basically, it considered any drop of 3% below 96% to be an indication of AHI), but I've been looking at numerous studies that have used 4% as the criteria. My lowest oxygen desaturation percentage was 93% (so 3% below). With a desaturation so close to what is considered normal (and considered normal by a number of other studies), I thought it strange that she would instantly jump to medical devices that I would need. This is especially true, I think, because while it measured my AHI as 9.4 (assuming that an AHI was a desaturation of 3% or more; if the measure was 4%, my AHI would have been zero, since my desaturation was never less than 93%), my ODI was 1.1. Just looking over about 3 studies comparing AHI and ODI, every one shows an extremely high correlation (r=95-98%) between AHI and ODI, which makes me confused as to why mine would be so drastically different.

With all of these things in mind, do you think that it's unreasonable for me to question the results of my study? Or do you think I'm just in denial and grasping at straws?

Sorry about the long post, and thank you to anyone that takes the time to read and reply.
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#2
You apparently had a simplified home sleep studiy that used the oxygen desaturation index as an indicator of potential sleep apnea. In this case the ODI used an unusually high threshold of significance based on a reduction of only 3% from baseline. Most of us experienced SpO2 levels well below 90% during the study. In addition, in the absence of a EEG during polysomography (PSG), periods of sleep cannot be distinguished from waking periods.

At best, your study should be considered a screening study. Before accepting any diagnosis based on those results, you should insist on a full clinical PSG, preferably as a 2-part study that includes titration in the event that obstructive sleep apnea is confirmed.
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#3
Ok, thank you. The hospital at which I did the study didn't seem to consider this a screening test at all and have given me a diagnosis of having sleep apnea without any further testing, and they wanted to try some (very expensive) appliances and machines.
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#4
I agree with Sleeprider. Also consider that you might have a related issue:
https://en.wikipedia.org/wiki/Upper_airw...e_syndrome

That would explain your daytime tiredness but lack of deep oxygen desaturations. UARS often turns into full flown OSA as people age. Both have some very serious, long-term effects on your health and you should get it checked out.

If you want to do some more reading, look up Dr. Steven Y Park. He has published a lot of layman-accessible information on these conditions.
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#5
Is UARS possible even though I have no snoring?
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#6
I agree with Sleeprider but a few of your other symptoms almost make it a slam dunk that you have sleep apnea or something that is interfering with your sleep. Tending to nod off in social situations is a good one. I used to nod off in meetings. I thought that I was just getting bored by the subject matter.

Did not get diagnosed with sleep apnea until I spent some time in the hospital with atrial fibrillation. The cardiologist at the hospital was the first to think of A-fib and recommend a PSG. Sure enough, I was bound to be a hosehead. I was in denial for some time but finally figured out that I was not smarter than everyone else. Plus my wife knew that I quit breathing sometimes during sleep. Now let's see. What is that called?? Oh yeah, I think that it is called sleep apnea.

A clinical PSG is a great idea if you have insurance that will pay for it. If not, you could see about a home sleep test.

Best Regards,

PaytonA
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#7
I actually was wondering if I had something similar to narcolepsy without cataplexy, as I think I have some of the other symptoms (hallucinations as I fall asleep, frequent sleep paralysis when I wake up, have vivid dreams during short naps). But if I could have a more definitive sleep study, whose results I didn't find a little disconcerting, that said I have sleep apnea, I certainly wouldn't object to finally finding a treatment to let me get through the day.
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#8
Adassai, You have a couple practical options here. You can accept the diagnosis based on this limited data, obtain the prescription for an auto-CPAP and start therapy. The major auto CPAPs (Resmed Airsense 10 Autoset and Philips Dreamstation Auto) provide very good data that will let you self-titrate the pressure and see if you have continuing events. If you feel better using CPAP, perfect. This could work for you, and the CPAP data would likely answer most of your questions.

If you have good insurance with low deductible and copay costs, then a more complete sleep study would seem to be a good idea, particularly if you could do a split study, with the first-half being diagnostic, and the second-half evaluating CPAP treatment. The test you took does not appear to be very complete, even in the context of a home study. There are any number of reasons a small oxygen desaturation could occur without apnea. The results of your home study point to mild sleep apnea of an unspecified type. It could be entirely hypopnea, partially obstructive sleep apnea, or less-likely central apnea (lack of breathing effort). It could also be medication, breathing under covers or pillows etc. There may be some aspect of that test you have not told us, but it seems like its value would be mostly as a screening tool, rather than diagnostic. Treating sleep apnea is a big investment of your lifestyle and money. Better diagnostic information would seem to be appropriate. At least that's my 2-cents.

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#9
(11-16-2016, 10:40 PM)Adassai Wrote: Is UARS possible even though I have no snoring?
Short answer is YES.

It is possible to have UARS and OSA without a history of snoring.

I also want to offer a counter view point to this statement by Sleeprider:
Sleeprider Wrote:In this case the ODI used an unusually high threshold of significance based on a reduction of only 3% from baseline. Most of us experienced SpO2 levels well below 90% during the study.
One of the AASM standards for scoring hypopneas during an in-lab PSG is a drop of 50% in the flow rate that lasts for at least 10 seconds and is accompanied by an O2 desat of (only) 3% from baseline. And in fact, a hypopnea can even be scored without an O2 desat at all if the 10+ second 50+% drop in flow rate is associated with an EEG arousal. And because of these ways of scoring hypopneas, it is quite possible for a person to have OSA and not experience O2 desats that lead to SpO2 levels dropping below 90% during the study.

Back to Adassai's original question of whether his/her in-home sleep study results are reliable enough to accurately diagnose OSA (or the related UARS): This is a case of "When you hear hoofbeats, think of horses not zebras." Given the combination of daytime sleepiness and high ODI on the study, it's reasonable to conclude that OSA/UARS is the problem, or at least a major part of the problem. And other problems, such as narcolepsy, are typically diagnosed (here in the US) only OSA/UARS has either been ruled out OR the patient continues to experience daytime symptoms even though the OSA/UARS has been successfully treated with xPAP in terms of reducing the AHI/RDI to less than 5.

Finally I want to say something about observation:
Adassai Wrote:Just looking over about 3 studies comparing AHI and ODI, every one shows an extremely high correlation (r=95-98%) between AHI and ODI, which makes me confused as to why mine would be so drastically different.
Even when there is an extremely high correlation between two variables, there are so-called "outliers"---data points that just don't match the expected correlation. Why any particular outlier winds up being an outlier really depends on a lot of things that may not be that closely related to the two variables with the strong correlation.

I'll offer my own OSA diagnosis as an example of being an example of a statistical outlier:

In the US, Medicare requires a drop in the flow rate of 30% or more AND an associated SpO2 drop of 4% or more in order to score a hypopnea. In other words, if the SpO2 drop is only 3%, a hypopnea cannot be score no matter how long the reduced flow rate for the event lasts nor does an event that ends in a clear respiratory effort related arousal get scored (as anything) if the SpO2 does not drop by at least 4%. However, the AASM has come to believe that any event where the flow rate drops by 50% or more that is associated with either a 3% drop in SpO2 OR an EEG arousal OR both should be scored as a hypopnea.

Studies have shown that for most people it doesn't really matter which of the two definitions are used to score the Hs---the difference in their calculated AHI won't be statistically significant.

But in my case, the difference between how you score the Hs is extremely significiant: Under Medicare rules, my diagnostic AHI = 3.9 and I would not qualify for xPAP therapy at all because an AHI < 5.0 is considered normal. Under the alternative AASM standard for scoring hypopneas, my diagnostic AHI = 23.1, and I wound up with a diagnosis of moderate (not mild) OSA.

It took a lot of digging for me to really understand my sleep study results: The key part of the data was that none of my hypopneas had an SpO2 drop of 4%---every single one of the 78 hypopneas scored during the 4.75 hours of sleep during the test was a "hypopnea with arousal"---I aroused before the SpO2 had time to drop. It's also important to note that an "arousal" is not quite the same as an awakening. (As a side note, on a different CPAP forum, at the time I was diagnosed, there was a lot of discussion about whether my diagnosis should or should not have been UARS; but there was no difference in calling my UARS vs OSA since both are treated with xPAP and my insurance company was not questioning the diagnosis of moderate OSA because they did not insist on using Medicare rules.

In other words, I think a conversation with a sleep doc to discuss the results of the test is reasonable. I'm not sure that an additional test is completely warranted however. It could be that the real diagnosis ought to UARS instead of OSA, but the fact is that UARS is treated with xPAP just like OSA is. It could be that all the data (which we do not have) might explain why Adassai's ODI data appears to be an outlier, and a sleep doc with access to all the data may be able to explain whether the fact that the data has some outlier features is enough to say the test may be a false positive.
Questions about SleepyHead?
See my Guide to SleepyHead
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#10
(11-16-2016, 10:40 PM)Adassai Wrote: Is UARS possible even though I have no snoring?
Short answer is YES.

It is possible to have UARS and OSA without a history of snoring.

I also want to offer a counter view point to this statement by Sleeprider:
Sleeprider Wrote:In this case the ODI used an unusually high threshold of significance based on a reduction of only 3% from baseline. Most of us experienced SpO2 levels well below 90% during the study.
One of the AASM standards for scoring hypopneas during an in-lab PSG is a drop of 50% in the flow rate that lasts for at least 10 seconds and is accompanied by an O2 desat of (only) 3% from baseline. And in fact, a hypopnea can even be scored without an O2 desat at all if the 10+ second 50+% drop in flow rate is associated with an EEG arousal. And because of these ways of scoring hypopneas, it is quite possible for a person to have OSA and not experience O2 desats that lead to SpO2 levels dropping below 90% during the study.

Back to Adassai's original question of whether his/her in-home sleep study results are reliable enough to accurately diagnose OSA (or the related UARS): This is a case of "When you hear hoofbeats, think of horses not zebras." Given the combination of daytime sleepiness and high ODI on the study, it's reasonable to conclude that OSA/UARS is the problem, or at least a major part of the problem. And other problems, such as narcolepsy, are typically diagnosed (here in the US) only OSA/UARS has either been ruled out OR the patient continues to experience daytime symptoms even though the OSA/UARS has been successfully treated with xPAP in terms of reducing the AHI/RDI to less than 5.

Finally I want to say something about observation:
Adassai Wrote:Just looking over about 3 studies comparing AHI and ODI, every one shows an extremely high correlation (r=95-98%) between AHI and ODI, which makes me confused as to why mine would be so drastically different.
Even when there is an extremely high correlation between two variables, there are so-called "outliers"---data points that just don't match the expected correlation. Why any particular outlier winds up being an outlier really depends on a lot of things that may not be that closely related to the two variables with the strong correlation.

I'll offer my own OSA diagnosis as an example of being an example of a statistical outlier:

In the US, Medicare requires a drop in the flow rate of 30% or more AND an associated SpO2 drop of 4% or more in order to score a hypopnea. In other words, if the SpO2 drop is only 3%, a hypopnea cannot be score no matter how long the reduced flow rate for the event lasts nor does an event that ends in a clear respiratory effort related arousal get scored (as anything) if the SpO2 does not drop by at least 4%. However, the AASM has come to believe that any event where the flow rate drops by 50% or more that is associated with either a 3% drop in SpO2 OR an EEG arousal OR both should be scored as a hypopnea.

Studies have shown that for most people it doesn't really matter which of the two definitions are used to score the Hs---the difference in their calculated AHI won't be statistically significant.

But in my case, the difference between how you score the Hs is extremely significiant: Under Medicare rules, my diagnostic AHI = 3.9 and I would not qualify for xPAP therapy at all because an AHI < 5.0 is considered normal. Under the alternative AASM standard for scoring hypopneas, my diagnostic AHI = 23.1, and I wound up with a diagnosis of moderate (not mild) OSA.

It took a lot of digging for me to really understand my sleep study results: The key part of the data was that none of my hypopneas had an SpO2 drop of 4%---every single one of the 78 hypopneas scored during the 4.75 hours of sleep during the test was a "hypopnea with arousal"---I aroused before the SpO2 had time to drop. It's also important to note that an "arousal" is not quite the same as an awakening. (As a side note, on a different CPAP forum, at the time I was diagnosed, there was a lot of discussion about whether my diagnosis should or should not have been UARS; but there was no difference in calling my UARS vs OSA since both are treated with xPAP and my insurance company was not questioning the diagnosis of moderate OSA because they did not insist on using Medicare rules.

In other words, I think a conversation with a sleep doc to discuss the results of the test is reasonable. I'm not sure that an additional test is completely warranted however. It could be that the real diagnosis ought to UARS instead of OSA, but the fact is that UARS is treated with xPAP just like OSA is. It could be that all the data (which we do not have) might explain why Adassai's ODI data appears to be an outlier, and a sleep doc with access to all the data may be able to explain whether the fact that the data has some outlier features is enough to say the test may be a false positive.
Questions about SleepyHead?
See my Guide to SleepyHead
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