Little Larissa - please read

General Discussion on any topic relating to CPAP and/or Sleep Apnea.
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Banned
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Post by Banned » Tue Apr 29, 2008 11:55 pm

dsm wrote: Re BPM rate. Auto is adequate for people who are not CAs sufferers.

Auto allows the machine to run like a bit like a spontaneous bilevel - but with the SV machine, it will react if the target of peak volume is not being met so that it will take over. i.e. If a CA occurs then the target of peak flowis not being met & within x time (I don't know what x is), the machine will take over & try to start ventilating.

The worrying aspect of how it does this is that I have repeatedly seen DLFO (from his data) stop breathing & the machine go to max pressure to try to inflate him be he still doesn't breath so the machine sits at 30 CMS (his IpapMax) and can do so for many minutes at a time.

Setting a BPM=12 (for example) would in DLFO's case cause the machine to cycle the pressure (servo ventilate) whenever DLFOs breathing rate drops below 12 breaths or if the target of peak flow is not being met.
So, you can turn Rise Time off as it is only a comfort measure? If you did set a Rise Time, what would it be for a 3-year-old?

How would you determine BPM if Auto, or a Back Up Rate (and what Back Up Rate) would be good for a 3-year-old with very challenging problems vs. a grown man who drank drano as a youngster? Wrestling with a BPM sounds like a recipe for disaster.

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Post by dsm » Wed Apr 30, 2008 1:33 am

Banned wrote:
dsm wrote: Re BPM rate. Auto is adequate for people who are not CAs sufferers.

Auto allows the machine to run like a bit like a spontaneous bilevel - but with the SV machine, it will react if the target of peak volume is not being met so that it will take over. i.e. If a CA occurs then the target of peak flowis not being met & within x time (I don't know what x is), the machine will take over & try to start ventilating.

The worrying aspect of how it does this is that I have repeatedly seen DLFO (from his data) stop breathing & the machine go to max pressure to try to inflate him be he still doesn't breath so the machine sits at 30 CMS (his IpapMax) and can do so for many minutes at a time.

Setting a BPM=12 (for example) would in DLFO's case cause the machine to cycle the pressure (servo ventilate) whenever DLFOs breathing rate drops below 12 breaths or if the target of peak flow is not being met.
So, you can turn Rise Time off as it is only a comfort measure? If you did set a Rise Time, what would it be for a 3-year-old?

How would you determine BPM if Auto, or a Back Up Rate (and what Back Up Rate) would be good for a 3-year-old with very challenging problems vs. a grown man who drank drano as a youngster? Wrestling with a BPM sounds like a recipe for disaster.

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What Are You Fixing (Reprise)?

Post by StillAnotherGuest » Wed Apr 30, 2008 5:38 am

-SWS wrote:Since Larissa's hypercapnia is presently considered secondary to obstructive apnea, her doctor just might want to briefly yet very safely trial Larissa in SV mode toward exploring a somewhat perplexing underlying etiology. BiLevel at 15/5 is not at all normally required for an obstructive apnea patient, let alone a pediatric case of OSA. There's more going on here than just basic OSA.
Boy, I'll say. And actually, the PSG suggests hypercapnia was aggravated by the administration of oxygen. Without knowing when they put the oxygen on or what the pattern of hypercapnia was without the administration of supplemental oxygen, I don't see how one could say that. The CO2 normally increases during night during different sleep stages, and normally administration of O2 shouldn't cause hypercapnia. Seeing the % of ETCO2 over 50 mmHg during the night would clarify that and determine if it's abnormal or not.

The OSA doesn't appear to be severe enough to generate hypercapnia. However...

It is not clear to me if in fact, she has central hypoventilation or alveolar hypoventilation (which does have obstructive etiology), and may be responsive to surgery:

Using Microstream® Capnography to Detect Alveolar Hypoventilation Syndrome in the Sleep Lab

Those hospitalizations look more like acute respiratory failure on chronic respiratory insufficiency (chronic hypercapnia). Yet, the limited ETCO2 data says that there was at least some time in the 40's, and nothing in the 60's. You need that ETCO2 detail to determine if it's central hypoventilation.

However, if the child had been effectively stabilzed with BiPAP over an extended period of time to "rest" the respiratory musculature (and we can argue that concept), there may be some residual reduction in pCO2.

Anyway, my guess in the pool is that BiPAP is being used to treat chronic respiratory insufficiency due to an underlying pulmonary or neurological issue. The ALTEs were not "out of the clear blue sky" but appeared with at least some warning (like worsening infection).

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The Infamous One More Thing

Post by StillAnotherGuest » Wed Apr 30, 2008 5:49 am

-SWS or RG was going to wrote:
Don't even think about it.
SAG
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Re: What Are You Fixing (Reprise)?

Post by -SWS » Wed Apr 30, 2008 6:49 am

StillAnotherGuest wrote:
-SWS wrote:Since Larissa's hypercapnia is presently considered secondary to obstructive apnea, her doctor just might want to briefly yet very safely trial Larissa in SV mode toward exploring a somewhat perplexing underlying etiology. BiLevel at 15/5 is not at all normally required for an obstructive apnea patient, let alone a pediatric case of OSA. There's more going on here than just basic OSA.
Boy, I'll say. And actually, the PSG suggests hypercapnia was aggravated by the administration of oxygen. Without knowing when they put the oxygen on or what the pattern of hypercapnia was without the administration of supplemental oxygen, I don't see how one could say that. The CO2 normally increases during night during different sleep stages, and normally administration of O2 shouldn't cause hypercapnia. Seeing the % of ETCO2 over 50 mmHg during the night would clarify that and determine if it's abnormal or not.
Well, that first part of the quoted text is not my own assessment. That's a summary of the PSG conclusion text. In that summary text the PSG-reviewing physician states the primary problem as OSA. She then goes on to evaluate hypercapnia with supplemental O2 as being a secondary problem. And she attributes that secondary problem as either an epiphenomenon commonly associated with OSA or as a direct and independent result of central hypoventilation. But she lists that condition as secondary, with OSA being primary (correct or incorrect as that assessment may be).

By contrast my last statement in the quote above clearly reflects that I think there's plenty more than just basic OSA going on. And you clearly think that as well.

Say, speaking of thinking...
StillAnotherGuest wrote:
-SWS or RG was going to wrote:
Don't even think about it.
SAG
Ya got your message boards all confused again! This is the one where people freely think and discuss. Remember?

Thought moderation... What a tough job on this message board!
Last edited by -SWS on Wed Apr 30, 2008 6:57 am, edited 1 time in total.

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Re: The Infamous One More Thing

Post by rested gal » Wed Apr 30, 2008 6:57 am

StillAnotherGuest wrote:
-SWS or RG was going to wrote:
Don't even think about it.
SAG
Me? I've only been wondering when the next marathon is...

Oh, and this too: "Ya gotta know what you're trying to treat, before you... etc."
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Post by -SWS » Wed Apr 30, 2008 7:15 am

Banned wrote:I have a co-worker breifly read Dr. Silvana's first report today. I was amazed he understood all of her medical terminology, and could explain to me the implications. I could not write or recall as fast as he was explaining. (He is a electrical/mechanical systems engineer). He was pretty amazed at that little report. There is allot in it and the details are pretty far reaching. He said he will try and spend more time with it and me tomorrow so I can write them down and post.
Banned, a real translation would be absolutely great! Please thank your colleague on our behalf! Do you think your colleague would mind also translating Dr. Silvana Simão's assessment that appears in the first post of this thread?

It sounds as if Dr. Silvana Simão thinks that central issues are primary. And I think that view differs from the PSG summary text---assuming the PSG summary text really does list OSA as Larissa's primary disorder.

I know that brazilian is tied up right now with travel. I'm sure he'll also kick in some translation assistance when he gets back.

Last edited by -SWS on Wed Apr 30, 2008 7:20 am, edited 1 time in total.

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What's A SAG, Anyway?

Post by StillAnotherGuest » Wed Apr 30, 2008 7:20 am

rested gal wrote:Me? I've only been wondering when the next marathon is...
LOL! OK, that'll only make it a 35,000 to 1 shot!

(OK, maybe 8000 to 1, if it's a good day).

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Re: What's A SAG, Anyway?

Post by -SWS » Wed Apr 30, 2008 7:22 am

StillAnotherGuest wrote:
rested gal wrote:Me? I've only been wondering when the next marathon is...
LOL! OK, that'll only make it a 35,000 to 1 shot!

(OK, maybe 8000 to 1, if it's a good day).

SAG
So which 35,000 people do you want us to detain?

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Re: The Infamous One More Thing

Post by -SWS » Wed Apr 30, 2008 10:09 am

rested gal wrote:Oh, and this too: "Ya gotta know what you're trying to treat, before you... etc."
Well, truth be told sleep medicine has historically treated multiple etiologies without knowing precisely what they were fixing. When medicine is forced to do this, treatment decisions are largely based on observation of experimental treatment challenges.

And some world-renowned experts in sleep medicine advocate diagnosing basic OSA based purely on home-trial CPAP or APAP. In the opinion of some very esteemed giants in sleep medicine, you really don't have to know what you're fixing before treating. Sometimes successful treatment challenges serve as the primary basis for diagnosis. And other times medical theory is at a pure loss regarding what they just fixed.

But I personally think it's preferable to diagnose before you treat. But what do I know? I'm just another one of those dumb patients.


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Post by ozij » Wed Apr 30, 2008 10:52 am

-SWS wrote:It sounds as if Dr. Silvana Simão thinks that central issues are primary.
Where do you get that from , -SWS? I couldn't find it in her first letter.
SAG really wrote:Those hospitalizations look more like acute respiratory failure on chronic respiratory
My guesses - google trantslator, and some knowledge of French coming to my aid:

On L.'s May 07 she was admitted with "partial sepsis" -(my comment: could be a result of a major respiratory infection of course). Since the first admission course with retention of CO2 demanding respiratory support, which necessitated her hopitalization in CTI (probably intesnive care) for 3 times.

At her last admission (11/07/2007) she presented with severe respiratory acidosis (PH 6.91, pCO2=241mmhg). At the time of her intubation she had a 3 minute cardiac arrest, but there was rapid return to spontaneous circulation. Permanently on mechanical ventilation till 18/08/2007 when she was extubated, and since then has been having apneas during sleep which cause drops (quedas) in the O2 saturation (My emphasis, O.).

It is my (O's) impression from the text that the severe hypercapnia and/ or hypoxemia occur only when she sleeps, (she's been in the hospital since Aug. 07 because of that) and the doctor wants to avoid those with the requested equipment.
(so(m)no --> somnolence --> sleep).

Last sentence in the PSG report:

"The SaO2 remained over 90% for more than 90% of the time, however without oxygen levels fell to 71%."

O.

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Post by -SWS » Wed Apr 30, 2008 12:29 pm

ozij wrote:
-SWS wrote:It sounds as if Dr. Silvana Simão thinks that central issues are primary.
Where do you get that from , -SWS? I couldn't find it in her first letter.

Perhaps very bad interpretation on my own part, ozij. Or at the very least, my own guess at what Dr. Silvana Simão conveys is psychologically biased by my own interpretive views.

However, my view is that what you transcribed below is a ventilatory response issue of undetermined etiology. I suspect this pathology has absolutely nothing to do with standard obstructive apnea as the primary cause (despite the PSG summary text that seems to indicate OSA as primary). Larisa's inadequate ventilatory response is a central issue, regardless of the pathogenesis (there's my own interpretive bias peeking out once again---albeit potentially an incorrect bias).

Please bear in mind that I find it highly doubtful that standard obstructive apnea causes this particular pathology, entailing such inadequate ventilatory response. And I also suspect recurring major respiratory infection would have routinely returned corroborative blood panel results, that would have been conveyed in these reports.



Not at all your standard OSA, and yet very clearly an inadequate central ventilatory response is involved here:
ozij wrote: My guesses - google trantslator, and some knowledge of French coming to my aid:

On L.'s May 07 she was admitted with "partial sepsis" -(my comment: could be a result of a major respiratory infection of course). Since the first admission course with retention of CO2 demanding respiratory support, which necessitated her hopitalization in CTI (probably intesnive care) for 3 times.

At her last admission (11/07/2007) she presented with severe respiratory acidosis (PH 6.91, pCO2=241mmhg). At the time of her intubation she had a 3 minute cardiac arrest, but there was rapid return to spontaneous circulation. Permanently on mechanical ventilation till 18/08/2007 when she was extubated, and since then has been having apneas during sleep which cause drops (quedas) in the O2 saturation (My emphasis, O.).

It is my (O's) impression from the text that the severe hypercapnia and/ or hypoxemia occur only when she sleeps, (she's been in the hospital since Aug. 07 because of that) and the doctor wants to avoid those with the requested equipment.
(so(m)no --> somnolence --> sleep).

Last sentence in the PSG report:

"The SaO2 remained over 90% for more than 90% of the time, however without oxygen levels fell to 71%."

O.
I haven't thrown CCHS out the window just yet as long as we're all guessing. CCHS is a central disorder that can be concomitant with obstructive apneas. Of course, not to confuse concern and conversation with attempts at treating via message-board quarterbacking. No one can or should treat this kind of case via a message board IMO.

I still think it's great when message board posters routinely straighten out inadequate OSA xPAP settings (since that real-world problem happens so often according to very many anecdotal posts requesting help). But Larissa's case doesn't come close to being anything of that simple nature. I personally think it's great for us to discuss and learn and care about Larissa.

And she may go home soon thanks to Banned, brazilian, and others!


P.S. Thanks for that text translation, O!

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Post by ozij » Wed Apr 30, 2008 1:14 pm

However, my view is that what you transcribed below is a ventilatory response issue of undetermined etiology.
Agreed.

I would assume that when the child's docotor says "obtructive apnea" they're using it descriptively (as an operational term) not diagnostically.

Her brain scan show some tissue reduction (athrophy?) which could be the result of hypoxia or its cause (poor muscular control manifesting itself during sleep? SDB can be an early indication of some degenerative neurological diseases - I don't know about children and those diseases).

Sepsis - can cause major harm to many systems, so my absolute layperson's hypothesising can wonder if the first bad infection caused her such grave harm that she no longer breathes properly at night.

Altrenatively (furthermore?), additional neurological harm may have happened during that 3 minute cardio/respiratory arrest - in any case after sending her home twice they are now keeping her in the hospital till she get breathing support for home use.

The way I read it, the child may certainly have a neurological disorder that is causing obstuctive apneas with major desaturations - maybe her brain doesn't jolt her out of sleep soon enough. Those have to be treated to keep her from further harm. (I'm not even hinting at which treatment is right). This may be in addition to hipoventilation.
Please bear in mind that I find it highly doubtful that standard obstructive apnea causes this particular pathology, entailing such inadequate ventilatory response. And I also suspect recurring major respiratory infection would have routinely returned corroborative blood panel results, that would have been conveyed in these reports.
Not necessarily, since the aim of these specific reports it to get her the equipment she needs for her obstructive apnea the aeitiology of which is unknown to us and irrelevant to the fact that she needs to be proprely oxygenated when she sleeps.
I haven't thrown CCHS out the window just yet as long as we're all guessing. Of course, not to confuse concern and conversation with attempts at treating via message-board quarterbacking. No one can or should treat this kind of case via a message board IMO. <snip> But Larissa's case doesn't come close to being anything of that simple nature. I personally think it's great for us to discuss and learn and care about Larissa.
Absolutely.

O.

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Post by -SWS » Wed Apr 30, 2008 1:29 pm

Great points IMO, ozij.
ozij wrote:Sepsis - can cause major harm to many systems, so my absolute layperson's hypothesising can wonder if the first bad infection caused her such grave harm that she no longer breathes properly at night.
Well sepsis can cause acidosis. And central blood-gas chemoreceptors in the brain are pH based. So sepsis-based acidosis can presumably skew central breathing I would also think... albeit as a sepsis-based head-scratching layperson.

Molecular responses to acidosis of central chemosensitive neurons in brain

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Post by brazilian » Wed Apr 30, 2008 2:44 pm

Friends:

this is a quick one, in the middle of my training here, just to inform you all that I have arrived, and received all packages in perfect condition at the hotel.

I have not had the opportunity to read the recent posts, but will do it at night today.

Regards to all.

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