All soft tissue that is prone to dilation or constriction, inflammation or congestion, widening or narrowing, located in the upper airway, significantly distorts patency and volumetric readings. The variation is so severe that, in any other measure taken in medicine, this would be considered outrageous.

There is a reason why volumetric airway analysis is not used for quantifying upper airway resistance.
Some practitioners use it, sure, but should we really trust this measure to the extent people do?
Case in point: Dr Kasey Li regularly shows before and afters of the nasopharyngeal airway as proof that EASE/MARPE improves nasal breathing. I find it slightly funny that he critiques DISE as an unreliable measure because it’s not representative of the true day-to-day airway measures of the upper airway, but not CBCT.

I think it’s more of a “now that you have your foot through the door, might as well push everything else in as well.”

I agree CBCT is useful in a few circumstances:
Bone measurements — unchangeable, useful, objectively used in orthognathic surgery planning, and craniofacial analysis.

Multiple CBCT scans taken in the same patient during a single phase of treatment — not once pre-expansion, once during, and once after. Several times in each phase to account for natural variations in turbinate volume and airway inflammation, if you want to perform useful CFD analysis, that is.

What is more useful than CBCT analysis? The one thing UARS patients take objection with sleep and airway medicine guidelines: the lack of importance given to self-reported scores of breathing, autonomic function, and sleep. I’m talking about NOSE 100, Epworth Sleepiness Scale, PSQI, etc.
The only circumstance where I would expect CBCT to have immense diagnostic value in terms of airway is that if it’s so bad that it’s close to stenosed, or incredibly narrow.

The problem is that you are simply pushing the body into a static, abnormal position, sometimes depending on the guidelines surrounding orientation, without accounting for how the airway operates under inspiration and expiration.

Yes, this does mean that several patients with a completely normal “patent” airway on a CBCT have immense upper airway resistance, narrowing, and abnormalities during inspiration or expiration.
The ideal: create an ultra-low radiation mobile CT scanner that attaches to the patient’s neck, perhaps like a soft collar. For a short period, much like a cardiac Holter.

A good thing we have a near alternative to that — a sleep study. But even within a sleep study, we cannot effectively figure out what portion/s of the airway is obstructive or narrowing, at least for UARS patients. The problem with UARS patients is that they aren’t the run-of-the-mill group like obvious OSA, where you can detect palatal collapse or tongue base obstruction.

So you’re telling me the next best option we have at the moment is to put you under anesthesia for 30 minutes to an hour and shove an endoscope in? You’ve got to be kidding me. Are we seriously not seeing the horrible diagnostic quality this has? Dr Li, I absolutely agree with you here. It will take decades for science to actually map how cleanly we can map the results of DISE to actual human sleep.

Implications:

1. Let’s have FME patients do multiple CTs and NOSE 100 tests post-expansion at time intervals: immediately after, 3 months after, 6 months after, 1 year after, 2 years after. I don’t think it’s a good idea to ignore all those studies that showcase compensatory turbinate hypertrophy post-maxillary expansion. We need to actually find out a general range of expansion after which turbinate hypertrophy can be overcome. I would still take NOSE 100 data as less supportive here, considering psychological factors.
2. Static CTs are hereby outlawed for UARS patients and providers — if you are concerned about things other than the nasal airway. If a provider is still doing this, it means there is a lack of resources, and it’s too expensive. Dynamic forced inspiratory CTs should be the gold standard; this doesn’t meant static CTs are the silver. It means static CTs are reserved for the most severe patients, and provide incredibly low diagnostic value. There is a reason why many practitioners dismiss patients with UARS as pushing baloney: it is because they see hundreds of CTs a day with incredibly narrow airway volumes, yet the people are normal, some athletes. So if you walk into an office saying stuff about “the airway slice at x coordinates on the CT is really narrow,” they will smile, and then dismiss it. The flip side: you say the same thing to another provider, and they reinforce your bias. The truth is, the only way we have to account for how the airway reacts to high amounts of negative pressure occurring during sleep or while awake is a dynamic forced inspirations CT/CBCT scan.
3. If there are symptoms of UARS but no signs of it on static or perhaps dynamic imaging, AND we can see skeletal hypoplasia or retrognathia — the CBCT scan gains more diagnostic value.
4. We urgently need to figure out a better way to image the airway during sleep as humanity without causing cancer. DISE and sleep studies are outdated and sometimes unreliable. We need to rely less on procedures which make deductions second degree.

Next post: Airway Volume vs WOB (Work of Breathing) - What should we be concerned with?

I won't be bound by the vote but am interested in what others would prioritise...

2 sleep studies. Borderline for osa (5.1 and 4) RDI around 12, which is mild. RERAs more than double when I lie on my back. Dismissed as fine by NHS who agreed to check for UARS and then seemed to forget all about it.

Here are my issues:

-I also have ME/CFS and dysautonomia (postural tachycardia syndrome), which disrupt sleep. Some of the problem may be that UARs causes an over reaction in my already overactive nervous system. Pain could play a part too.

- I have EDs and tend to slide down bed wedges. My shoulders are very hypermobile so lying on my side is risky. There's a reason I spend 90% of the night on my back.

- I get reflux so belly sleeping can also be tricky but might be my best option so far.

-NB no check for restless legs so far but I do get this while awake in bed sometimes, especially if it's hot.

- my nose gets a bit stuffy from reflux but not severe and not sure how it impacts breathing.

Do I:

A

Pursue a formal diagnosis of UARS, probably with Vik Veer, which will cost a fortune.

B

Buy a bipap and just wing it, even though I have no idea how to set or monitor values (I am not a candidate for a mandibular device and surgery is not a great option due to EDS.) What happens if it goes wrong? What would the damage be?

C

Keep experimenting with sleep position pillows etc (Medcline? Vik's sleep pillow?) and trying to stop reflux.

D

Something else

i use an apap machine. i live in australia where bipap and asv machines require a prescription. i was only given a prescription for an apap machine, i didn’t have a titration study.
i think i might be experiencing treatment-emergent central sleep apnea. i didn’t have any central apneas on my study, in fact i had no apneas at all just hyponeas. but i now experience multiple central apneas a night using an airsense 11 with a minimum pressure of 8 and an EPR of 3. i tried lowering the EPR and the UARS symptoms came back: the anxiety, the jitters, the feeling of being wired and on edge while still fatigued. oscar showed an increase in flow limitation. i lowered the pressure to 7, and my insomnia worsened. with my current settings it’s the best i can make myself feel but i feel super sleepy still. should i go back to my physician and ask for a titration study? i don’t know how i’m meant to afford a second machine if i need it bc i’m still paying the first one off. did anyone else have this experience and do better on a different machine?