I have been diagnosed with UARS now after tonsillectomy and two sleep studies. Had moderate to severe sleep apnea prior to surgery.  I know these could be basic questions, but any input would be great.

1. I now have cpap wide open at 4cc of pressure to 20cc of pressure  7 day average 10.8 cc of pressure..ahi of 5.
    If i didn't have UARS/sleep apnea the pressure would stay at 4cc not an average of 10.8 cc.  The reason I asked this is
    because my sleep doc in Portland (I am working with Stanford now) said I don't need cpap.  Just use the tap three
    because you need the jaw pulled out and cpap doesn't work well with UARS.  Again Portland doc and Stanford doc think
    two different things.

2. Does dental appliances work better then cpap in treating UARS.

3. Has any one out there been diagnosed with sleep apnea (rdi 42 ahi of 28) and then had Tonsils/uppp ect and been diagnosed with UARS.  

Scott

Treatment for UARS

Although a mild decrease in airflow while sleeping may not seem like a big problem, it has been shown to disrupt sleep enough to cause and/or perpetuate CFS/FMS. Therefore, keeping your airways open can be critical.30

Over the years a simple nasal dilator called Nozovent (available online) has proved to be one of the most popular and easy to use devices to enhance nasal breathing. This device is not just for snorers but can be used by anybody who suffers from nasal resistance. Another easy option is "Breathe Right" nose strips. These are available at most pharmacies and many supermarkets. Also, a prescription nasal spray called the "Sinusitis Nose Spray" that combines itraconazole (Sporanox), xylitol, mupirocin (Bactroban), and dexamethasone is available by mail order from the ITC compounding pharmacy (see resources - appendix F in FFTF). It is often very effective at treating the nasal congestion and sinusitis that can trigger UARS. Just as your physician to call in the prescription for 1 bottle of the "Sinusitis Nose Spray" to ITC at 303-663-4224. Use 1-2 sprays in each nostril for 2 x day. When the bottle is done, it can be used as needed, so most patients keep an extra bottle on hand as a spare. My sinusitis and nasal congestion patients LOVE IT, and it may help the UARS to go away.

I would try each of these for one month and even try all three together, if necessary, and see how you feel. If they do not help, you may wish to consider CPAP or an oral appliance.

Continuous Positive Airway Pressure (CPAP) is often one of the first recommendations a doctor will make for this condition. The CPAP delivers air into your airway through a specially designed nasal mask that prevents your nasal passages from collapsing. Oral appliances to move the jaw forward can also help, and in some severe cases, surgery on the soft palate or even to widen narrowed jaw bones may be necessary. Because the obstruction is mild, sometimes a newer ,gentler machine that uses nose prongs instead of a mask can be used. Eliminating or even treating the UARS can markedly improve your function!

http://www.endfatigue-dev.com/articles/Article_uars.html

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It appears as though physicians differ on how to treat UARS. Some want to shoot directly at CPAP, while others are more willing to go with oral devices first. Its up to you. CPAP will probably treat it well, if you can tolerate it, and save you money in the long run.

Cpap is the best treatment, but not the most tolerated. Compliance rates are awful. If you have any doubts, I would go with the recommendation in the article. Just my opinion.

Hi Scott sleep,

I am also a sleep patient at Stanford.  I have OSA (in the form of all hypopneas, just a stray apnea every now and again), and UARS as shown by sleep study with PES.  I've had two such studies at Stanford.

The CPAP machine's algorithms can handle the detection of OSA fairly easy, but UARS can be a little more troublesome.  Some CPAPs have more and varied flow limitation sensors than others, and the sensing accuracy can vary from machine to machine as well.  My Stanford doctor felt the Repsironics M Series Auto (the prior model with C-Flex, not the newer A-Flex model) that I have, was as good a choice as any other when it comes to UARS.

My titration was not hugely accurate due to my severe insomnia, pressure was determined for treating OSA but UARS remained a wildcard.  Based on the incomplete titration we started with a range of 8-12 (titration magic number was 10), the machine tended to run to 11 and this controlled the OSA (AHI ranged 2.2-4.4 over several months).  Stanford doctor suspected UARS was still largely untreated (gut feel and experience I believe), and over time changed the range to 10-14, then 12-14, it is now at a fixed pressure of 14.  

This seems to work very well for OSA with AHI 0-1.1 and she suspects the UARS is also being controlled.  I will have a repeat sleep study in the near future to assess my RDI vs. AHI.  (My untreated AHI was 53.6 while my RDI was 83.6.)  According to my Stanford doctor, a sleep study is the only real way to measure if the UARS is under complete control at pressure 14, since my machine can't reliably detect or measure it.

I don't know how true this holds for others, this is what my situation and experience are so far.  Perhaps your situation will be similar.

Also, my airway constriction is well below the base of my tongue, the length of my airway relaxes and collapses on itself.  There is no surgery or applicance that can address this type of constriction.   CPAP is the magic bullet.

Blessings,
--pseudonym

I should add, my tonsils and adenoids were out when I was a kid, and that is long ago I do not have a small jaw or thick tongue, and no palate obstruction.  My nasal breathing is open and clear with the exception of the occasional colds/flu.  I do not have allergies.

Did Stanford use a PES to diagnose UARS?  If so that could mean your restriction is below tongue level as mine is, and you'll need to use a CPAP to treat it.  No nasal or oral appliance can influence this area.

Blessings,
--pseudonym

Thank you so much for the reply.  You have helped me a great deal.  I am considering the MMA surgery and will fly down again for the second time to meet with the surgeon and discuss the sleep study in more detail.  I will tell you this doc is the greatest doc I have met so far.  He doesn't promote surgery and makes it clear 1. cpap first 2 dental appliance 3. then last resort surgery.  My specs  3mm throat size  1mm behind tongue when laying down small receded jaw and large tongue.  As you said though who knows it could be lower in the throat.  QUESTIONS

1.  Do you feel better with cpap?  I find it hard to keep on with any pressure higher then 10...I RIP IT OFF THREE HOURS INTO NIGHT  NOT KNOWING..

2.  Do you have a lot of stage shifts with and without  cpap/awakenings/arousals?  I hear bi pap also works well with UARS.  

3.  THANKS AGAIN FOR THE KIND RESPONSE!!!!!!!  Sorry to be forward, but how did you know the obstruction was below you're tongue?  This is why I AM HESITANT TO DO MMA SURGERY.

SCOTT

Hi Scott,

In my case the PES monitor was the helpful factor.  That's why I asked you:  Did you have a sleep study at Stanford with PES?  PES is pressure monitor for lower in your throat.  A small catheter is threaded into one nostril and down into the throat.  A machine similar to an IV pump is attached, it discharges fluid (usually saline or water) at intervals throughout the night and records the pressure.  You would know if you had this done   It isn't painful but it is not the most pleasant thing I've ever experienced!

I had a sleep study (no PES) before the Stanford one with PES.  That prior sleep study found nothing responsible for the reason I was there: Severe insomnia.  They found no sleep apnea, no limb movements, no respiratory disturbances.  They did show hundreds of stage shifts but failed to identify a cause.  I spent 70%+ of my typical 2-3 hours sleep in stage 1, with the balance in stage 2.  No slow wave (deep) sleep and no REM (dream) sleep.  That explains the severe fatigue and mental fog I had!

Since no cause was found, my doctor and I tried many different sleep aids and other drugs such as anti-depressants, that might be helpful.  Most of these did not work for me at all, including all but one of the sleep aids.  Lunesta was one that did work, at first, but after 8 months it gradually stopped being effective and by one year it no longer made a difference.  That was when I got my referral to Stanford.  I was out of options.

I have not had any problem with the CPAP pressure, once I got the mask I have now.  Even though I'm not a mouth breather and breathe fine through my nose, I now have a full face mask. (I originally wanted to get a FFM just to have on hand for colds, but it fit so much better it has become my full time mask.) It is a Hans Rudolph 7600.  I have the older version, new version is called the 7600 V2.  My mask works very well but I have reports from others who have the V2, the V2 has some good improvements over my mask.

I tried many nasal cushion masks and nasal pillows masks (over a dozen) before I found the Hans Rudolph 7600.  The pressure was only 11 then and was very uncomfortable for me with nasal cushions or pillows.  I also suffered aerophagia (swallowing air) and was very bloated and uncomfortable within a short period of using the CPAP.  The highest C-Flex setting helped quite a bit with that, but now that I use the HR FFM, I don't use C-Flex at all.

I also don't use a ramp, and don't use a humidifier.  (I do have an Aussie Heated hose for the cold wintertime air.) I start right out with pressure 14.  It feels like almost nothing with the HR FFM (with nasal cushions and pillows even 11 felt like a gale).  Since I take a very long time to fall asleep, Stanford has allowed me to break the 'good sleep hygiene' rules and climb into bed an hour or more early.  I don mask and turn on the blower, and I read a book or listen to soft music or podcast.  When I'm ready to fall asleep I just turn out the light from right where I am.  I am lucky, I do not have to get up during the night, so the mask stays on a full 8 hours whether I am awake and reading a book, or asleep.

Regarding the bi-level, that seems to be a very individual thing.  Me and the bi-level, we are not compatible     One was tried during my tiration to see if it would help with the aerophagia I had experienced (and it should).  But my breathing pattern is too erratic, and I end up fighting the machine and cannot 'sync up' with it.  This is turn made me more alert and eventually wide awake, I was too frustrated to sleep.  Now that I have the HR FFM, I do not have aerophagia even at pressure 14 and no exhale relief.

Regarding ripping the mask off unconsciously.  This is a well documented 'feature' of some new CPAP users.   Some people have had success at leaving the mask alone by scolding themselves about it, just before bed.  No kidding, that worked for quite a few.  You can also use skin-friendly wound or medical tape (not the bandage adhesive tape of the last century!) and tape your mask to your face in several places.  This is often enough of a reminder to your subconscious to leave the mask on.  If you do awaken and find you've taken it off, just put it back on and go back to sleep.  Do that even if it is almost time to get up.  If you don't want to put it back on, then just get up early.  Don't go back to sleep without it.  In time you'll leave it alone.

I personally do not think that running an auto CPAP 'wide open' provides the best therapy for many (most?) people.  I am not a doctor, but my own experience, plus what others have shared with me, indicate that a very narrow range or a fixed pressure yields better therapy.  Ask your doctor about whether restricting the APAP to a 4-5 point spread (or less) would work better for you.  You might also look into a different mask, one that will disperse the CPAP air and reduce the feeling of pressure.
 
Do check into the PES, and see if that is warranted as a diagnostic for you.  Also, if you haven't done it aleady, be sure to get a copy of your full sleep studies (5-6 pages with graphs, not just the 1-2 page summary letter from the doctor).  Your last sleep study detail could tell you quite a bit more about where you're 'at' today in this.

Blessings,
--pseudonym

Hello "pseudonym".

Can you tell me the difference between UARS and OSAS.

I have read some of the post in this Forum, and some articles on the Internet. But I still don't understand the difference.

Henning

Henning wrote:

Hello "pseudonym".

Can you tell me the difference between UARS and OSAS.

I have read some of the post in this Forum, and some articles on the Internet. But I still don't understand the difference.

Henning

Not to invade on pseudonym, but a clear cut definition is here:

Pathophysiology of UARS is similar to obstructive sleep apnea / hypopnea syndrome in that abnormal airway resistance in the upper airway during sleep leads to unwanted physiologic consequences. Increased upper airway resistance in this disorder does not lead to cessation of airflow (apnea) or decrease in airflow (hypopnea), but instead leads to an arousal secondary to increased work of breathing to overcome the resistance.

Hi Henning,

Upper Airway Resistance Syndrome was a Stanford discovery and research continues to be pioneered by Stanford.  Not all the major sleep medical universities and hospitals agree that it exists, however.  Stanford continues to diagnose and treat UARS successfully.

My case was not typical as I have both hypopneas and UARS, pure OSA and pure UARS patients have differing characteristics and I don't really fit into either category discretely

As I understand it, UARS is not objectively measured, it is detected as one of the flow restrictions or respiratory disturbances with arousal, that results in a RERA scoring but not an AHI scoring.  Pure UARS presents a high RERA but little or no AHI.  Many of the shared elements between OSA and UARS present differently, for example UARS is typically silent whereas OSA is often (but not always!) accompanied by snoring.  Pure UARS patients tend to weigh less than OSA patients and have slower or no weight gain within the previous 5 years.  Pure UARS tends to present with the highest degree of mental and psychological impairment, the highest degree of insomnia, the highest degree of complaints regarding sleep quality, abnormal sleep cycles and stage shifts, and the highest degree of residual daytime sleepiness.  Pure UARS is less likely to result in O2 desats than OSA, and is more likely to be accompanied by high blood pressure.

My untreated AHI is 53.6 and my RERA is 83.6.  No objectively measured cause of the residual disturbance of 30 could be determined, e.g. no limb movements, no cardiac events, no O2 desats (a stray apnea did drop my O2 to 87% for 1.5 seconds; however my mean O2 was 95%), no snoring.  I was very fit back then from regular body building and aerobics, with low-normal blood pressure and a slow steady heart rate indicative of aerobic fitness.  Stanford examined the differences in my clinical presentation from OSA and that is what led to an additional Dx of UARS.

There are many good articles on UARS (and on the debate as to whether it exists).  Search the trusted clinical research sources such as PubMed, MedScape, Medline, Journal of Sleep Medicine, etc.  and you should turn up quite a few.

Blessings,
--pseudonym

Thank you RAM_Sleep, you got in there while I was typing     It pays to be brief!

Excellent synopsis to what I just detailed in my novel.  Thanks again!

Blessings,
--pseudonym

pseudonym wrote:

Hi Henning,

Upper Airway Resistance Syndrome was a Stanford discovery and research continues to be pioneered by Stanford.  Not all the major sleep medical universities and hospitals agree that it exists, however.  Stanford continues to diagnose and treat UARS successfully.

My case was not typical as I have both hypopneas and UARS, pure OSA and pure UARS patients have differing characteristics and I don't really fit into either category discretely

As I understand it, UARS is not objectively measured, it is detected as one of the flow restrictions or respiratory disturbances with arousal, that results in a RERA scoring but not an AHI scoring.  Pure UARS presents a high RERA but little or no AHI.  Many of the shared elements between OSA and UARS present differently, for example UARS is typically silent whereas OSA is often (but not always!) accompanied by snoring.  Pure UARS patients tend to weigh less than OSA patients and have slower or no weight gain within the previous 5 years.  Pure UARS tends to present with the highest degree of mental and psychological impairment, the highest degree of insomnia, the highest degree of complaints regarding sleep quality, abnormal sleep cycles and stage shifts, and the highest degree of residual daytime sleepiness.  Pure UARS is less likely to result in O2 desats than OSA, and is more likely to be accompanied by high blood pressure.

My untreated AHI is 53.6 and my RERA is 83.6.  No objectively measured cause of the residual disturbance of 30 could be determined, e.g. no limb movements, no cardiac events, no O2 desats (a stray apnea did drop my O2 to 87% for 1.5 seconds; however my mean O2 was 95%), no snoring.  I was very fit back then from regular body building and aerobics, with low-normal blood pressure and a slow steady heart rate indicative of aerobic fitness.  Stanford examined the differences in my clinical presentation from OSA and that is what led to an additional Dx of UARS.

There are many good articles on UARS (and on the debate as to whether it exists).  Search the trusted clinical research sources such as PubMed, MedScape, Medline, Journal of Sleep Medicine, etc.  and you should turn up quite a few.

Blessings,
--pseudonym

Hi pseudonym!

Thank you for your answer.

I have now read other articles. I also found out that UARS is accepted in Denmark. (They use the Stanford method as well).

As I understand it, my CPAP machine will not record these UARS (or RERA episodes) – apart from AHI also will score on the RERA score?

Therefore an Auto CPAP can’t do anything to these episodes. You have to use a fixed pressure to manage these RERA?

Is that assumption correct?

Henning

No, I don't think that assumption is correct.  

Pressure is not correlated with severity or type of flow restriction.  It is whatever pressure YOU require to keep YOUR airway open sufficient to stop the events and associated arousals and sleep distruptions.  This is highly individual.  Some people with severe SDB require low pressures while others with mild SDB require very high pressures.  And everything in between.

I suspect this is true with UARS as well.  Some people require less, the same, or more pressure than what controls their OSA (if they also have OSA).  As the machine cannot reliably detect UARS it also has no information as to whether UARS is being effectively treated (or not) at the current pressure(s).  UARS could be well controlled, there is just no way to know one way or the other from the machine data.  To say the "auto cannot do anything to these episodes" is incorrect; PAP therapy controls UARS, the Auto function simply cannot detect them and therefore cannot attempt to treat them by raising or lowering the pressure.

In my particular case we moved toward a fixed pressure simply because an auto range exacerbates my insomnia.  Any little thing (and often it seems like nothing at all!) can talk me out of sleeping, often for the remainder of the night.  I have never used the ramp, as I didn't care for it, but that too would have been a problem.  The noise and airflow sensation from the auto changing pressure, and from exhale relief, would either prevent me from falling asleep or awaken me constantly throughout the night.  The HR FFM eliminated the aerophagia and therefore the need for exhale relief, and fixed pressure eliminated the sound of the auto changing pressures.  

As far as I am aware, the ONLY way to detect UARS (or the lack of it) is with an in-lab sleep study.  There is no method or in-home equipment that can track it or measure treatment success with CPAP.  I strongly recommend against any self-prescribed pressure changes, up or down, in an attempt to diagnose or treat RERAs that occur in addition to OSA, as there can be no facts associated with what those pressure changes are or aren't doing for the RERAs.  Not to mention the change of pressure may reduce or eliminate effective therapy for OSA if present, or induce central apnea if raised too high.

If you, or anyone reading here, have any concerns about UARS or untreated RERAs occuring with successful treatment for SA, it would be a good subject to broach with your sleep specialist at the earliest convenience.  These RERAs are just as disruptive as OSA to good health.  The sooner correct and effective treatment is determined and initiated, the better.

Blessings,
--pseudonym

Well – as I can see – this is very complicated.

After I have got my coblation on my turbinate’s, I’m going to have a new sleep study – including this PES monitoring (This is also the way to see if you have inspiratory / expiratory apneas – negative or positive pressure in esophageal).

I certainly will insist of this examination for UARS too.

Henning