My DCS Hit

[Nitrogenius]

Your junk method is adding 16 overlapping pieces of information, and it does not factor or scale off the diminishing harmless surface values. As a result, the serious part of the dive where the injury is created is made small, while the harmless surface part is made large. The surface part is all useless information, as it can be infinitely big and still be harmless. But the dive part is the only part that matters.

While they occur on the surface, they were seeded in the dive.

You can't create surface supersaturation on its own, that is detrimental (except for air travel). Detrimental surface supersaturation must follow on from a dive. If a DCS has occurred (for reasons of gas pressure stress - not a thousand other usual things), then insufficient deco time was the cause. Hence the surface ISS is of no consequence to discovery of the correct amount and placement of deco stops.

Wow Ross !
At least I have to give that to you.. You are able to surprise again and again.
This statement here clearly proves that you actually do not understand the genesis and pathology of DCS at ALL!
Impressive..

 

[Simon Mitchell]

The surface supersaturation under normal conditions, is in continuous decline - the ideal scenario for tissue micro-bubble reduction.

...and...

the surface ISS level does not matter

Absolute nonsense, demonstrably false, and further evidence that your knowledge of this field is extremely poor.

So supersaturation during the dive matters, but after the dive it doesn't? Given that supersaturation is simply a physical state, tell me how a developing bubble senses when it is at the surface so that (under your paradigm) the bubble somehow knows it should no longer form or grow and magically stops doing so because surface supersaturation does not matter?! Supersaturation is supersaturation whether it occurs during or after the dive, and it will drive bubble formation whether it occurs during or after the dive. Just because it begins to decline after the dive does not mean it won't drive bubble formation any more.

Indeed, bubbles are often absent during monitoring early after dive, and only peak during prolonged monitoring at the surface. A recent review of appropriate strategies for monitoring post dive bubbles [1] had this to say (the bits in bold are the key in relation to this discussion):

From these data, representing nine different studies with varying dive profiles, it can be seen that there is great variation in the time of onset, peak and disappearance of Doppler detectable VGE across individuals and across dive profiles. It appears obvious that every dive profile cannot uniformly be characterised by monitoring VGE within a short time period of between 30 and 60 minutes, or even up to 90 minutes post-dive.

Take, for example the data reported in Figures 7 and 8. Here the subjects performed the same dry chamber dive compressing to 18msw for 100 minutes then decompressing in accordance with RN Table 11. The difference between the dive protocols was a period of exercise taken two hours before compression in one instance while the other dive acted as a no-exercise control. Doppler measurements made between 30 and 60 minutes would have missed the median peak bubble grades after both dives. The control dive produced its median peak grades at 75 to 90 minutes, while the median peak for the dive with pre-dive exercise occurred at 105 minutes.

These findings are completely incompatible with your senseless idea that supersaturation at the surface does not matter. It is clear that bubble formation gains momentum at the surface - because Ross, there is time for the supersaturated gas to form bubbles or diffuse into existing ones (there's that integral of time and supersaturation thing again). There are many other studies that show the same trend for bubble formation to peak well after arrival at the surface, across all types of dives including recreational no decompression dives (eg [2]).

A NDL diver has a tiny amount of surface ISS, but still develops a DCS... from the dive event

What!!? What do you mean "from the dive event"? Someone swimming around at 18msw for 40 minutes (a NDL diver) who then surfaces over 2 minutes will experience virtually ALL of their supersaturation (which I would not refer to as "tiny") after arrival at the surface. If they suffer DCS then it is because of this post-surfacing supersaturation. Honestly Ross, you are losing the plot. You have no place commentating on these matters as a self proclaimed expert.

Simon M

1. Blogg SL, Gensser M. The need for optimisation of post-dive ultrasound monitoring to properly evaluate the evolution of venous gas emboli. Diving Hyperb Med 2011;41:139-46.

2. Dunford RG, Vann RD, Gerth WA, Pieper CF, Huggins K, Wacholz C, Bennett PB. The incidence of venous gas emboli in recreational diving. Undersea Hyperb Med 2002;29:247-59.

 

[rossh]

Absolute nonsense, demonstrably false, and further evidence that your knowledge of this field is extremely poor.

So supersaturation during the dive matters, but after the dive it doesn't? Given that supersaturation is simply a physical state, tell me how a developing bubble senses when it is at the surface so that (under your paradigm) the bubble somehow knows it should no longer form or grow and magically stops doing so because surface supersaturation does not matter?! Supersaturation is supersaturation whether it occurs during or after the dive, and it will drive bubble formation whether it occurs during or after the dive. Just because it begins to decline after the dive does not mean it won't drive bubble formation any more.

Indeed, bubbles are often absent during monitoring early after dive, and only peak during prolonged monitoring at the surface. A recent review of appropriate strategies for monitoring post dive bubbles [1] had this to say (the bits in bold are the key in relation to this discussion):

From these data, representing nine different studies with varying dive profiles, it can be seen that there is great variation in the time of onset, peak and disappearance of Doppler detectable VGE across individuals and across dive profiles. It appears obvious that every dive profile cannot uniformly be characterised by monitoring VGE within a short time period of between 30 and 60 minutes, or even up to 90 minutes post-dive.

Take, for example the data reported in Figures 7 and 8. Here the subjects performed the same dry chamber dive compressing to 18msw for 100 minutes then decompressing in accordance with RN Table 11. The difference between the dive protocols was a period of exercise taken two hours before compression in one instance while the other dive acted as a no-exercise control. Doppler measurements made between 30 and 60 minutes would have missed the median peak bubble grades after both dives. The control dive produced its median peak grades at 75 to 90 minutes, while the median peak for the dive with pre-dive exercise occurred at 105 minutes.

These findings are completely incompatible with your senseless idea that supersaturation at the surface does not matter. It is clear that bubble formation gains momentum at the surface - because Ross, there is time for the supersaturated gas to form bubbles or diffuse into existing ones (there's that integral of time and supersaturation thing again). There are many other studies that show the same trend for bubble formation to peak well after arrival at the surface, across all types of dives including recreational no decompression dives (eg [2]).



What!!? What do you mean "from the dive event"? Someone swimming around at 18msw for 40 minutes (a NDL diver) who then surfaces over 2 minutes will experience virtually ALL of their supersaturation (which I would not refer to as "tiny") after arrival at the surface. If they suffer DCS then it is because of this post-surfacing supersaturation. Honestly Ross, you are losing the plot. You have no place commentating on these matters as a self proclaimed expert.

Simon M

1. Blogg SL, Gensser M. The need for optimisation of post-dive ultrasound monitoring to properly evaluate the evolution of venous gas emboli. Diving Hyperb Med 2011;41:139-46.

2. Dunford RG, Vann RD, Gerth WA, Pieper CF, Huggins K, Wacholz C, Bennett PB. The incidence of venous gas emboli in recreational diving. Undersea Hyperb Med 2002;29:247-59.

Look at Mitchell deliberately confuse intra vascular and extra vascular micro bubbles... again. Dopppler / VGE is NOT tissue micro-bubbles or DCS. You have been told this by your peers in a consensus (1).

You are a doctor - stop making shit up.


1. Consensus_guidelines_for_the_use_of_ultrasound_for_diving DHM

.

 

[rossh]

Why don't you publish your "obvious and simple" conclusions in a journal. Writing a paper would take a fraction of the time spent arguing on the internet.

Or Kevin / Simon could publish thier version of ISS method after formal testing / verified / validated / calibrated for stress relevance and risk assessments.

See... you want to let them get away with anything that suits them, but refuse to have them prove their case. No double standards here - except for Mitchell. He has free license to redefine biological processes, decide what comprises stress, and ignore the reality when his deco ideas run off the rails.

.

 

[Nitrogenius]

Look at Mitchell deliberately confuse intra vascular and extra vascular micro bubbles... again. Dopppler / VGE is NOT tissue micro-bubbles or DCS. You have been told this by your peers in a consensus (1).

You are a doctor - stop making shit up.


1. Consensus_guidelines_for_the_use_of_ultrasound_for_diving DHM

.

The absurdity continues.. Where can I get this stuff you seem to be on ross? It is pretty obvious that Simon is not confusing anything.
It is as well consens that there is a strong correlation between VGE counts and general decompression stress and hence the likelihood of DCS to occur..
consensus is lesser VGE count lesser DCS risk more VGE count more DCS risk.. oh btw this is not calibrated so maybe it must be let me guess "junk science"
you will not like it but the correlations there are likely similar to correlations between ISS and DCS risk..

 

[Brett Eldridge]

In this same meeting Bruce from shearwater research mentioned that they had or were changing the default GF setting on their computers to 30/70 instead of, I believe it was, 15/85 (but I can not remember exactly).

I wasn't at that meeting, but I'm pretty sure the default went from 30/85 to 30/70 around the time the Perdix started shipping (i.e., only the GF hi changed).

I'm looking forward to Innerspace 2019 and hoping to hear more discussions like this -- already signed up!

- brett

 

[LionFi2s]

Just wondering....
1. If Don had submitted his dive profile to the database Rossh keeps without making this report, how would someone know the outcome and if it was an uneventful dive or not? Someone could claim that 60/70 works fine too.
2. Is there anyone else besides Rossh that still advocates for the deep stop approach? Preferably a relevant scientist
3. Are there any recent studies that show an advantage of the bubble models over a shallower stop approach?

Speedy recovery Don and thanks a lot for sharing!

 

[Michael Thornton]

I wasn't at that meeting, but I'm pretty sure the default went from 30/85 to 30/70 around the time the Perdix started shipping (i.e., only the GF hi changed).

Looking at an old shearwater GF manual (Version 3) at the beginning of the manual where it uses Eric Bakers graph to explain GF settings it says the default is 30/85 and further into the manual where it explains how to change conservatism it says the default is 15/85.

 

[Brett Eldridge]

Looking at an old shearwater GF manual (Version 3) at the beginning of the manual where it uses Eric Bakers graph to explain GF settings it says the default is 30/85 and further into the manual where it explains how to change conservatism it says the default is 15/85.

Interesting. I think when I started diving with Shearwaters, they had already moved to 30/85 but hadn't yet changed the default to 30/70.

I was just reading a manual for one of their newer computers (Teric) that has an "OC Rec" mode and it stated that the default GF in that mode is "medium (40/85)" whereas in the "OC Tec" or "CC/BO" modes it is a "more conservative 30/70."

- brett

 

[rossh]

Just wondering....
1. If Don had submitted his dive profile to the database Rossh keeps without making this report, how would someone know the outcome and if it was an uneventful dive or not? Someone could claim that 60/70 works fine too.
2. Is there anyone else besides Rossh that still advocates for the deep stop approach? Preferably a relevant scientist
3. Are there any recent studies that show an advantage of the bubble models over a shallower stop approach?

Speedy recovery Don and thanks a lot for sharing!

These deep dives, often have a consultation period, before, during and after with numerous parties involved. But in any case, the big ones often find their way into the public forum no matter what, as they often include some record or place of interest and support team.

DIR and RD still exist, still deeper than VPM-B, and still very popular use. RGBM too. The deeper stop approach is the most sucessful and has the lowest injury rates for the 16+ years its has been in use.

There are no studies that show an advantage either way that are valid for purpose or compelling.. But lots of gross miss interpretations by interested parties favoring the shallow side though.

.

 

[rjack]

The deeper stop approach is the most sucessful and has the lowest injury rates for the 16+ years its has been in use.
.

Could you provide some peer-reviewed literature to support this conclusion please? Asking for a friend.

 

[Simon Mitchell]

Look at Mitchell deliberately confuse intra vascular and extra vascular micro bubbles... again. Dopppler / VGE is NOT tissue micro-bubbles or DCS. You have been told this by your peers in a consensus (1).

You are a doctor - stop making shit up.


1. Consensus_guidelines_for_the_use_of_ultrasound_for_diving DHM

.

I am not confusing anything, but you are. We measure VGE in decompression research because they move in blood vessels and can be detected using Doppler ultrasound or echocardiography. We can't readily detect tissue bubbles. Based on physiological first principles it is virtually certain (and substantially proven) that higher numbers of VGE are associated with a greater tendency for tissue bubble formation. In contrast, your idiosyncratic claim is that the tendencies for VGE formation and tissue bubble formation are somehow unrelated. But there is not a single diving physician in the world who thinks that the drivers for bubble formation in tissue capillaries and in the tissue itself are unlinked. That notion is just a magical construct you have concocted to dismiss the importance of VGE because in just about every context in which VGE are discussed in these debates, it debunks one of your weird ideas (like my post above where the continued formation of VGE after a dive debunks your claim that supersaturation after a dive doesn't matter).

It is nothing short of bizarre that you continue to cite the consensus guidelines on ultrasound monitoring in decompression research as somehow supporting your inference that VGE don't matter. Please explain to me Ross, why would a group of academics expend considerable effort generating a consensus guideline on how to measure something irrelevant? The entire purpose of that paper is to define optimal methodology for measuring VGE as an index of decompression stress after diving. Which brings me back to my ealier post....

These findings (peak VGE formation long after surfacing) are completely incompatible with your senseless idea that supersaturation at the surface does not matter. It is clear that bubble formation gains momentum at the surface - because Ross, there is time for the supersaturated gas to form bubbles or diffuse into existing ones (there's that integral of time and supersaturation thing again). There are many other studies that show the same trend for bubble formation to peak well after arrival at the surface, across all types of dives including recreational no decompression dives (eg [2]).

Are you still trying to claim that supersaturation at the surface doesn't matter?

Simon M

 

[Simon Mitchell]

Could you provide some peer-reviewed literature to support this conclusion please? Asking for a friend.

PLEASE drill Ross down on his claim that "the deeper stop approach is the most sucessful and has the lowest injury rates for the 16+ years its has been in use".

My own belief is that there are no reliable data whatsoever describing rates.

You could also ask him about the outcomes of the published human studies formally comparing deep and shallower approaches. If Ross is not forthcoming I can post summaries and references for these studies which should satisfy your friends curiosity.

Simon M

 

[Simon Mitchell]

Or Kevin / Simon could publish thier version of ISS method after formal testing / verified / validated / calibrated for stress relevance and risk assessments.

The case for ISS is already proven to a level that is entirely satisfactory for the purpose to which we are putting it. Read David Doolette's posts that you have been linked to.

Mitchell. He has free license to redefine biological processes, decide what comprises stress, and ignore the reality when his deco ideas run off the rails.

Actually Ross, this is exactly what you do in your Gish-galloping posts. My presentation of all matters in these debates is based on facts or strongly supported inferences from the diving science literature, some of which is my own, but most contributed by my colleagues. Since you are fond of denying the obvious, you will claim my views don't reflect the current science. Readers will have to judge the plausibility of such a claim for themselves.

In relation to Ross's claim that I am "making shit up" about the pathophysiology of DCS, and at the risk of sounding self indulgent, I must point out that I am teaching the pathophysiology of DCS on a DAN Course for doctors at St Lucia in 2 weeks. In October I am teaching the same topic to the NOAA DMO course in Seattle. I have been teaching on these courses for years. I wrote the chapters on DCS pathophysiology for the current editions of all 3 major diving medicine textbooks (referenced here). I am the incoming Editor in Chief of Diving and Hyperbaric Medicine - the worlds highest ranked peer reviewed diving medicine journal. Ross will whine about "Appeal to Authority", but he is making extraordinary accusations about me, and given my roles in the scientific community the gross implausiblity of his claims is an obvious and important part of the prima facie defence of those accusations.

Simon M

 

[rossh]

I was talking to Neal Pollock, back in May at the TekDiveUSA. We were talking about VGE and other related stuff and how they evolve.. Neal made the strong comment "No one knows were VGE come from".. But I guess what he should of said is: "No one knows were VGE come from, except Simon.".

.

 

[Simon Mitchell]

I was talking to Neal Pollock, back in May at the TekDiveUSA. We were talking about VGE and other related stuff and how they evolve.. Neal made the strong comment "No one knows were VGE come from".. But I guess what he should of said is: "No one knows were VGE come from, except Simon.".

I agree. Nobody knows exactly how or where VGE form, although the tissue capillaries are by far the most likely place and there is some direct evidence that bubbles form there, but what's your point? The indisputable fact is that bubbles appear on the venous side of the circulation, and their preponderance can only reflect the supersaturation state of the tissues through which the blood passes. The arterial blood entering the tissues, having just passed through the lungs and equilibrated gas tensions with ambient pressure, is not supersaturated at all. Bubbles appear on the venous side and can only do so if the tissues are supersaturated, and the preponderance of those bubbles will be directly proportional to tissue supersaturation.

Just so that we don't leave any loose ends, can you answer my previous question just for the record? In light of the discussion above, do you still believe that surface supersaturation doesn't matter? Or are you going avoid answering and to hope that you can leave that one behind like you have tried to pretend your claim (on scubaboard) that tissue perfusion doesn't influence gas kinetics didn't happen?

Simon M

 

[rossh]

Could you provide some peer-reviewed literature to support this conclusion please? Asking for a friend.

There is 5 papers / places so far that will help you. No single one will give you the full answer so you need to read between the lines a little.

Some papers below are from memory and I'm not going to dig up the references because you are not interested anyway - just trying to wind me up.

DAN yearly dive reports.
BSAC yearly dive reports, broken down by dive groups too.
A case review study report for 10 years in Netherlands, published in UHMS
An Australian 12 year case study of cave divers I think - DHM.
Simon's Kiwi study of cases too - DHM.

Anyway, they all show declines in injury numbers / etc.


The worst years we had for DCS was around 2000, at the end of the shallow stop / USN table era. We have been in decline ever since, but it remains to be seen if Simon Mitchell's "new, more efficient" deco method, actually does anything better.

 

[rossh]

I agree. Nobody knows exactly how or where VGE form, although the tissue capillaries are by far the most likely place and there is some direct evidence that bubbles form there, but what's your point? The indisputable fact is that bubbles appear on the venous side of the circulation, and their preponderance can only reflect the supersaturation state of the tissues through which the blood passes. The arterial blood entering the tissues, having just passed through the lungs and equilibrated gas tensions with ambient pressure, is not supersaturated at all. Bubbles appear on the venous side and can only do so if the tissues are supersaturated, and the preponderance of those bubbles will be directly proportional to tissue supersaturation.

Just so that we don't leave any loose ends, can you answer my previous question just for the record? In light of the discussion above, do you still believe that surface supersaturation doesn't matter? Or are you going avoid answering and to hope that you can leave that one behind like you have tried to pretend your claim (on scubaboard) that tissue perfusion doesn't influence gas kinetics didn't happen?

Simon M

The scuba board discussion was about how tissue models work. They have no adjustments for perfusion.... But of course you used to opportunity to distort my comment out of context,.... as usual the only way you win arguments is to screw with people.



For extra vascular tissue micro bubble growth ( that's NOT VGE Simon). the injury is initiated in the dive or at the end of the dive. The controlling factor and solution is deco time which naturally has follow on surface supersaturation (continuously declining).

The surface ISS number you cook up is not relevant, and cannot predict risk or stress.

.

 

[AdrianSmith]

Randy Thornton - I am concerned at two things in this thread:

1. The discussion has devolved on Ross’ side to a series of ad hominem attacks against Simon, UWSojourner, Nitogenius and others. They provide solid evidence to support their hypotheses, and Ross responds by personally insulting them and denigrating their professional reputations. This isn’t helping anyone, nor is it advancing the discussion on deco models. We appear to be stuck in a loop, as often happens when Ross goes into rant mode.

2. I’m concerned at the false equivalence that’s being created. Ross may constantly scream “fake news” with no data to back up his claims but he does so incredibly aggressively and it may lend an air of validity to his claims in the eyes of some.

I have been away from reading technical diving forums for approximately three years, although not from diving. When I last read RBW it was a thread in which Ross was spitting venom and I decided I didn’t need to be a part, however passive, of his hatred. I came back to CCR Explorers based on your post on FB, and lo and behold it’s the exact same nonsense and vitriol from him. I don’t believe this helps the technical diving community, nor does it show respect for basic human dignity. All it does is let us watch a slow motion car crash over and over. I don’t believe he deserves a platform for his anger and hatred and ignorance.

I would like to formally ask that at this point the moderators ban Ross from the forum. He is in direct violation of the forum terms of use, which states:

“You agree to not use the Service to submit or link to any Content which is defamatory, abusive, hateful, threatening, spam or spam-like, likely to offend, contains adult or objectionable content, contains personal information of others, risks copyright infringement, encourages unlawful activity, or otherwise violates any laws.“

Ross has violated this time and again with his defamatory, abusive and hateful content, and I believe it is well past time to ban him.

Thank you,
-Adrian

 

[UWSojourner]

I was talking to Neal Pollock, back in May at the TekDiveUSA. We were talking about VGE and other related stuff and how they evolve.. Neal made the strong comment "No one knows were VGE come from".. But I guess what he should of said is: "No one knows were VGE come from, except Simon.".

Dr. Pollock and Ross have interacted before and here are a few other things Dr. Pollock has said.

Link
"Intravascular bubbles are not the perfect measure, but they provide insights that certainly are not discounted in the scientific community. Similarly, they should not be discounted in the diving community."

Link
"Unfortunately, Ross, I do not believe that our core positions are in agreement. The differences are much greater than simply semantic."

Link
"It is not valid to talk about microbubbles in the bloodsteam as different from microbubbles in any other tissue."

Link
"If the research community had any reason to believe the genesis of bubbles was wildly different between blood and non-blood tissue, we would probably have some evidence at this point. We do not."

Link
"... a fundamental element that is common to all bubble models of decompression ...Not one of them measures bubbles. Not one. There is theorizing and hand waving, but no measures. Despite this, the near-religious fervor is often felt."

Link
"Bubbles are a clear indicator of decompression stress. Getting off the bottom (that is, skipping the deep stops) can reduce tissue loading in intermediate and slow tissues. No matter what is done at depth, prolonging shallow stop time is effective at reducing VGE in individuals predisposed to develop them. Other strategies might work, but I am most impressed by those based on credible evidence. I call prolonged shallow stops really cheap insurance."

Link
"The impact of deep stops is not that they target some different physical reality. It is actually quite simple; the extra time spent deep allows more inert gas uptake in the relatively undersaturated intermediate and slow tissues. This is simply a loading problem that subsequently produces a higher degree of decompression stress. If there is less uptake at depth, ascent to a relatively shallow stop has much less risk. The idea that deep stops controlled bubble growth is one of the armchair arguments that has not lived up to human testing ... As with all the protocols we developed and subsequently saw fail, it is time to respect the data over the hand-waving."

Link
"For the record, the work of Simon Mitchell is really easy to review. It is almost always well-developed, appropriately interpreted, and clearly presented. He is a major asset to the medical, research and diving communities."

Link
"The story is advancing nicely. Simon [Mitchell] has provided a number of solid references that describe some of the relevant current understanding ..."