Cutting Edge Bubble study indicates possible damage to circulatory system

[rossh]

That is what is interesting about this study Ken. (At least to me!) I think there has always been some level of discussion going on about exactly how the bubbles were destructive and incredulous as it may sound, there seems to be some people who still feel that there is no direct correlation between bubbles and DCS. For me, the big question that remains is whether the damage caused by bubbles at a cellular level is permanent in anyway.

Hi Randy.

Sorry to interrupt this thread with VGE talk, but you keep baiting me to join with stuff like....


"....some people who still feel that there is no direct correlation between bubbles and DCS."


Randy, That statement is correct. Here is some expert opinions on this:

From the latest Consensus development conference on the subject of VGE: Recommendation 11: Fair interpretation: Interpretation of bubble data should be appropriately constrained, for a number of reasons: • bubbles do not equal DCS; .....

Neal Pollock says similar things in his DCS stress presentations: warns against the direct correlation remarks - slide.

Under those same consensus guidelines above, David Doolette tried to bring the nedu 192 dive, shallow stop test, to a positive conclusion on VGE - it failed to achieve this; Diving and Hyperbaric Medicine 46 (1) VGE detected by two dimensional echocardiography are an imperfect endpoint for DCS. From the conclusion... VGE cannot be used to diagnose DCS, but it can be used for comparisons of procedures....

I have another paper from the Bruback group (2012?), in which they put the VGE to DCS direct correlation at just 4%.


Randy, this "direct correlation" notion, is simply not true. VGE can be used as a general average of stress, but it cannot be used as an absolute measure. i.e compare within a single profile for a general level of stress, but is still a weak measure.


You might like to know, one can reduce their VGE by as much as 84%, through pre-dive vibration. Pre-dive Whole-Body Vibration Better Reduces Decompression-Induced Vascular Gas Emboli ...

Imagine; I have lower VGE than you, because I drive a bumpy pick up truck to the dive site, and you drive a Mercedes? So if individuals can influence at will their VGE score by a 5:1 factor, then what does it say about the worth of VGE?


The biomarker rat test discussed here, suffers from the same vagueness issues of DCS It says: "The total bubble count for each rat varied widely between the animals at each time point (Figure 1B)", and "However, bubble formation showed significant variability even among rats with low weight variation and with decompression at the same rate, with coefficient of variation ranging from 34% to 79% between the three subgroups. This finding coincides with observations that individual variation in DCS susceptibility exists in divers 19,30. "

We know VGE and deco stress occur concurrently, but not in any predictable ratio. We also know a lot of combined stresses will cause a DCS, but we also know that VGE is not the cause of DCS in most people.

Still today, no one really knows why, or where, or how VGE grow. Until these important questions are answered, please do not be tempted to over-hype the value of VGE. The underlying message of the consensus paper above, was to avoid doing this.


*******************

Back to the thread topic:


There are two decompression rates used in the test - one is almost a direct ascent - it shows significant deviations in biomarkers (RD group). The other deco rate, was a bit slower, and has almost no change in biomarkers (SD).. It's a fine line between the groups.

Ascent rates: (44ft to 66ft/min for RD group, 16ft/min for SD group).

The paper says; "Linear regression revealed a significant positive relationship between decompression rate and bubble formation (Fig. 2B)."

Are the bubbles and damage because of animal studies have driven decompression beyond the failure point, to something that is guaranteed to create a DCS? A direct ascent and skipped deco is already known to be bad every time.

A rat has 0.4% the body mass of a human, and I think its unlikely to be able to make rats decompress with the same onset of VGE, as we see in humans. I imagine its difficult to animal test the human condition - Normal VGE that are present in all of us, but are not causing us a DCS incident.

***

I think some readers have been missing some important benefits of these tests. In part, it is providing bio-markers to show that a DCS has occurred. This may well lead to something that the the hyperbaric doctor can test for, before deciding how much treatment to provide. Currently the diagnosis for DCS is very limited. How often does the emergency room leave DCS patients waiting and untreated, because they don't believe the patient story for urgency? A positive blood test would give confidence towards a speedy treatment.

.

 

[Randy Thornton]

Hi Randy.

Sorry to interrupt this thread with VGE talk, but you keep baiting me to join with stuff like....


"....some people who still feel that there is no direct correlation between bubbles and DCS."


Randy, That statement is correct. Here is some expert opinions on this:

From the latest Consensus development conference on the subject of VGE: Recommendation 11: Fair interpretation: Interpretation of bubble data should be appropriately constrained, for a number of reasons: • bubbles do not equal DCS; .....

Neal Pollock says similar things in his DCS stress presentations: warns against the direct correlation remarks - slide.

Under those same consensus guidelines above, David Doolette tried to bring the nedu 192 dive, shallow stop test, to a positive conclusion on VGE - it failed to achieve this; Diving and Hyperbaric Medicine 46 (1) VGE detected by two dimensional echocardiography are an imperfect endpoint for DCS. From the conclusion... VGE cannot be used to diagnose DCS, but it can be used for comparisons of procedures....

I have another paper from the Bruback group (2012?), in which they put the VGE to DCS direct correlation at just 4%.


Randy, this "direct correlation" notion, is simply not true. VGE can be used as a general average of stress, but it cannot be used as an absolute measure. i.e compare within a single profile for a general level of stress, but is still a weak measure.


You might like to know, one can reduce their VGE by as much as 84%, through pre-dive vibration. Pre-dive Whole-Body Vibration Better Reduces Decompression-Induced Vascular Gas Emboli ...

Imagine; I have lower VGE than you, because I drive a bumpy pick up truck to the dive site, and you drive a Mercedes? So if individuals can influence at will their VGE score by a 5:1 factor, then what does it say about the worth of VGE?


The biomarker rat test discussed here, suffers from the same vagueness issues of DCS It says: "The total bubble count for each rat varied widely between the animals at each time point (Figure 1B)", and "However, bubble formation showed significant variability even among rats with low weight variation and with decompression at the same rate, with coefficient of variation ranging from 34% to 79% between the three subgroups. This finding coincides with observations that individual variation in DCS susceptibility exists in divers 19,30. "

We know VGE and deco stress occur concurrently, but not in any predictable ratio. We also know a lot of combined stresses will cause a DCS, but we also know that VGE is not the cause of DCS in most people.

Still today, no one really knows why, or where, or how VGE grow. Until these important questions are answered, please do not be tempted to over-hype the value of VGE. The underlying message of the consensus paper above, was to avoid doing this.


*******************

Back to the thread topic:


There are two decompression rates used in the test - one is almost a direct ascent - it shows significant deviations in biomarkers (RD group). The other deco rate, was a bit slower, and has almost no change in biomarkers (SD).. It's a fine line between the groups.

Ascent rates: (44ft to 66ft/min for RD group, 16ft/min for SD group).

The paper says; "Linear regression revealed a significant positive relationship between decompression rate and bubble formation (Fig. 2B)."

Are the bubbles and damage because of animal studies have driven decompression beyond the failure point, to something that is guaranteed to create a DCS? A direct ascent and skipped deco is already known to be bad every time.

A rat has 0.4% the body mass of a human, and I think its unlikely to be able to make rats decompress with the same onset of VGE, as we see in humans. I imagine its difficult to animal test the human condition - Normal VGE that are present in all of us, but are not causing us a DCS incident.

***

I think some readers have been missing some important benefits of these tests. In part, it is providing bio-markers to show that a DCS has occurred. This may well lead to something that the the hyperbaric doctor can test for, before deciding how much treatment to provide. Currently the diagnosis for DCS is very limited. How often does the emergency room leave DCS patients waiting and untreated, because they don't believe the patient story for urgency? A positive blood test would give confidence towards a speedy treatment.

.

Ross, I'm sorry you feel that I have baited you to join the conversation. That was certainly not my intention. I would only say the following: Because we do not fully understand the correlation between bubbles and DCS does not mean that there is not a correlation between the two. As I mentioned previously, I'm not a doctor nor am I a research scientist, but to simply ignore the fact that there appears to be bubbles present in virtually all DCS cases would be fool hardy in my opinion. As I mentioned in my initial couple of posts, it is interesting to me to see how the bubbles are affecting the circulatory system and perhaps gain further insight into potential causes of DCS.

 

[kwinter]

I hope we all keep in mind that correlation is not the same as causation. Post hoc ergo propter hoc is hardly ever true. But I am interested in the Bruback study Ross mentioned because I am unaware of anything that shows a correlation level as low as 4%. I certainly thought correlation was much, much higher, and that both DCS and bubbles could have a common progenitor.

 

[rossh]

.....t, but to simply ignore the fact that there appears to be bubbles present in virtually all DCS cases would be fool hardy in my opinion. As I mentioned in my initial couple of posts, it is interesting to me to see how the bubbles are affecting the circulatory system and perhaps gain further insight into potential causes of DCS.

There is bubbles in almost every DCS, because almost every DCS usually involves some kind of higher tissue stress, higher off gas rates, or some form of profile / procedure error. ie. too fast and too much off gassing. There is more dissolved gas in motion, in a shorter period of time under those conditions. Naturally the VGE creation process (what ever it is), goes into fast mode as well.

The basic method to avoid a DCS, is to lower tissue stress levels and lower off gas rates... but VGE are still present, in almost all dives. VGE have been with us in diving for 45 years. We have all been ignoring them ever since, or in some cases, we acknowledge they exist and happily dive with them anyway.

Please don't get it backwards....VGE will exist, with or without a DCS sized stress event.

****

Do we aim to avoid DCS? Or avoid VGE?

The first one is the important, obviously. But trying to avoid the second one is rather futile, as VGE exist in almost every dive, regardless of the ascent or model used. They also exist in recreational divers, free divers, people who exercise, and many others.

So with that reality in mind, and the given the theory that all VGE can cause some form of injury, then where are the patients?

There are individuals today with a lifetime of diving experience behind them. There are professionals who dive 6 days a week for a job, all with VGE in their system every day.. What short or long term health issues can we see in them from VGE? Do we see or suspect poor health or unique illness trends in these people that's caused by VGE? No. So please keep that in mind when obsessing about a VGE levels.

 

[rossh]

I hope we all keep in mind that correlation is not the same as causation. Post hoc ergo propter hoc is hardly ever true. But I am interested in the Bruback study Ross mentioned because I am unaware of anything that shows a correlation level as low as 4%. I certainly thought correlation was much, much higher, and that both DCS and bubbles could have a common progenitor.

From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258401/

"VGE can be seen in large amounts without any commensurate manifestation of decompression injury (Nishi et al. 2003). However, the risk of DCS increases with the amount of bubbles detected (Eftedal et al. 2007a). In his masters thesis, Sawatzky (1991) systematically analyzed maximum Doppler scores and DCS incidence in a total of 3,234 dives. He found only one incidence of DCS not accompanied by detectable bubbles, giving a negative predicting value of 0.999 and a sensitivity of detectable bubbles as a test for DCS of 0.99. However, Sawatzky also detected bubbles without any symptoms of DCS, which gave a positive predictive value of only 0.04. This illustrates that having detectable bubbles yields only a 4% chance of developing DCS. Even when using high bubble grades as test criterion, the positive predictive value is low (Eftedal 2007). As Eftedal (2007) stated in his doctoral thesis: “.. the absence of detectable bubbles is a good indicator of decompression safety, but the occurrence of bubbles, even high grades, is a poor predictor of decompression sickness”. Since there seems to be only a statistical relationship between VGE and DCS, the detection of bubbles by ultrasound can not be used as diagnostic criteria for DCS."

 

[uwxplorer]

From https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258401/

This is an interesting review, but it goes a little bit in all directions. In particular, in its concluding remarks, it says:
"Even though many questions still exist, the damaging effects of these bubbles on the endothelium are well documented. We suggest that this is a central mechanism in the development of serious DCS, and further that it can be a mechanism for the possible long-term health effects of diving."
It could be argued that this is exactly what the original paper posted by Randy is saying.

For me, the two sentences that best summarize the review are these:
"Even in animal experiments, where physiological variables are tightly controlled, there is a considerable and significant difference in response between individuals. The same dive can produce few or many bubbles, and the response to bubbles differs as well."

So are the individuals the confounding factors, or are bubbles an essentially irrelevant readout?

 

[emmbee]

I hope we all keep in mind that correlation is not the same as causation. Post hoc ergo propter hoc is hardly ever true. But I am interested in the Bruback study Ross mentioned because I am unaware of anything that shows a correlation level as low as 4%. I certainly thought correlation was much, much higher, and that both DCS and bubbles could have a common progenitor.

That 4% figure is just the probability of having DCS if you have any bubbles. Actually it's not "the" probability, it's one of many, from a study in 1991. This study puts it at 6% for the grade 1 "one bubble once in a while" category.

It says nothing about how increasing the amount of bubbling impacts that probability. That the correlation between amount of bubbling and DCS is loose, even at high bubble grades, is unsurprising (to me, anyway) because, one, bubble grades are a blunt instrument, and, two, they "measure" (ahem) total body bubbling whereas DCS is a local effect. A lot of bubbles coming from your whole body, but only a few from each part is not the same thing at all as a lot of bubbles coming from just one part. Guess in which case you're more likely to overload your body's ability to cope?

One last thing, about 4% being characterised as “low”. Let’s imagine the dive profile you run always produce bubbles. Without further information, just using that p(DCS|bubbles)=4% probability, what’s the probability that you’ll do 50 dives without DCS? (1-4%) ^ 50 = 13%. Doesn’t seem so low anymore, does it?

The only thing that’s low about a 4% risk is the chances of making it in one piece if you keep doing it!

Arguing that some bubbling is fine because "it's just 4%" is nonsense. Never mind "good".

Cheers,

Matthieu

 

[kwinter]

That 4% figure is just the probability of having DCS if you have any bubbles. Actually it's not "the" probability, it's one of many, from a study in 1991. This study puts it at 6% for the grade 1 "one bubble once in a while" category.

It says nothing about how increasing the amount of bubbling impacts that probability. That the correlation between amount of bubbling and DCS is loose, even at high bubble grades, is unsurprising (to me, anyway) because, one, bubble grades are a blunt instrument, and, two, they "measure" (ahem) total body bubbling whereas DCS is a local effect. A lot of bubbles coming from your whole body, but only a few from each part is not the same thing at all as a lot of bubbles coming from just one part. Guess in which case you're more likely to overload your body's ability to cope?

One last thing, about 4% being characterised as “low”. Let’s imagine the dive profile you run always produce bubbles. Without further information, just using that p(DCS|bubbles)=4% probability, what’s the probability that you’ll do 50 dives without DCS? (1-4%) ^ 50 = 13%. Doesn’t seem so low anymore, does it?

The only thing that’s low about a 4% risk is the chances of making it in one piece if you keep doing it!

Arguing that some bubbling is fine because "it's just 4%" is nonsense. Never mind "good".

Cheers,

Matthieu

And once again I point to the difference between correlation and causation. A 4% correlation likely indicates that there is no relationship greater than mere coincidence. A 4% causation probability does indicate (as you pointed out) an 87% likelihood of getting DCS in the course of 50 dives.

 

[emmbee]

And once again I point to the difference between correlation and causation. A 4% correlation likely indicates that there is no relationship greater than mere coincidence. A 4% causation probability does indicate (as you pointed out) an 87% likelihood of getting DCS in the course of 50 dives.

And once again I have to point out that this is not a case of "correlation is not causation". I mean, I just did it on the previous page.

"correlation is not causation" reminds us that just because we have a correlation between A and B does not mean that A causes B. Indeed it could be:
- A indeed causes B
- a coincidence;
- B causes A
- C causes A and B
- both A causes B and B causes A

There's also the indirect ones...

Anyway. None of this applies because this 4% is not a correlation. Not in the scientific sense. A correlation is how two variables change with each other.

That 4% is not that. It's the positive predictive value, which in this case is #bubbly divers with DCS / #bubbly divers, which is also the conditional probability p(DCS|bubbles), the probability of having DCS if you have bubbles.

The correlation one could make out of this data is:
- without bubbles the probability of having DCS is 0.1%
- with bubbles the probability of having DCS is 4%

Which is actually a very good correlation, but a useless one because there's only 2 data points.

The number you're looking for, the one that "indicates that there is no relationship greater than mere coincidence", is called the p-value. The p-value is the probability that the null hypothesis (in our case, that it's random) come up with the same result (or a more extreme one). You should have seen this pop up in all the papers posted above. Usually in medical papers a p-value of less than 5% means that we can dismiss the null hypothesis.

So what is the p-value here?

Well it's (all picks without ordering):

(the number of ways to pick 1 bent non-bubbly diver out of all the non-bubbly divers) times (the number of ways to pick n bent bubbly divers out of all the bubbly divers) divided by (the number of ways to pick n+1 bent divers out of all the divers)
PLUS (this is the one more extreme case)
(the number of ways to pick 0 bent non-bubbly diver out of all the non-bubbly divers) times (the number of ways to pick n bent bubbly divers + 1 out of all the bubbly divers) divided by (the number of ways to pick n+1 bent divers out of all the divers)

The problem is we don't have all the figures. We just know that there's 3234 dives, at least 667 non-bubbly ones (to have 0.999, accounting for rounding), and that 4% of bubbly ones resulted in DCS. We don't know how many were bubbly or not - well, I don't, and the paper is not available online - anyone does? Ross?

What we can do, though, is try all the possibilities...

The maximum p-value is when we have 49 bubbly dives (out of 3234, remember), in which case the p-value is 2.7%. Which is still comfortably under the 5% threshold, no matter how ridiculous this scenario is considering the subject of the study.
Imagine a more reasonable scenario where half the dives were non-bubbly (I'd expect less in a study of doppler detected bubbles vs DCS), then the p-value is... 3.9 * 10^-21. So much for the null hypothesis.

So I think it's fair to say we can ignore the coincidence idea.

In our case, we have p(DCS|bubbles)=0.04 . If you have bubbles, there's a 4% chance that you have (or will have) DCS. It's that simple. Which of the causality options above is correct is irrelevant (except coincidence). "Correlation is not correlation" does not matter. Even if it turns out that actually DCS causes bubbles, we'll still have...

Assuming that 4% figure: if you do 17 bubbly dives, you have better than 50% chances to get bent at least once. If you do 50, its more than 87%.

So:

Pointing out that "it's just 4%" is fine to remind everyone that just because they've seen one bubble does not mean the diver needs to go into the pot.
Arguing that profiles that yield regular bubbling are fine because "it's just 4%" is nonsense. Never mind that it's actually a good thing.

Cheers,

Matthieu

 

[Randy Thornton]

Thank you Matthieu for making sense out of this for us mere mortals! The figures become a little more meaningful now, at least to me!

 

[uwxplorer]

Let's not forget that this "4%" figure is based on a suspicious lone observation mentioned in an unpublished master thesis.
Generally, this kind of citation raises red flags in science: extraordinary claims call for extraordinary care. There are such things as "outliers" in datasets, and the trick is to be able to provide all the details for a forensic analysis of what caused them: was this an experimental fluke or error (somebody bumped the measurement apparatus, the patient omitted to tell an important detail, etc) or is there indeed something unforeseen going on... If submitted for publication, I hope that this claim of an outlier would have been seriously questioned by reviewers... Since the master thesis was apparently not followed by a publication, the question was never asked.
But there is a special rule of review papers (which the paper brought up by Ross is): they are reviewed with different criteria than research papers, and sometimes "opinions" are tolerated if not encouraged.
As I mentioned earlier, the review lists pretty much everything and its contrary in terms of what could cause DCS (this is a review after all), so I would not put it as the same level as the original paper linked to by Randy. At least, it needs to be read critically. Like anything, if I may add.

 

[emmbee]

Thank you Matthieu for making sense out of this for us mere mortals! The figures become a little more meaningful now, at least to me!

Well I need to thank Ken for forcing me to (try to) make sense of it.

Let's not forget that this "4%" figure is based on a suspicious lone observation mentioned in an unpublished master thesis.

I would assume that this was a study of studies. I entirely agree that this figure should not be taken as gospel.

Cheers,

Matthieu

 

[kwinter]

Well I need to thank Ken for forcing me to (try to) make sense of it.
Cheers,

Matthieu

Yass, thank you Matthieu for the clarification. It saved me from digging out my stats texts to refresh on W-values and t-tests. Your comments are dead on.

 

[Simon Mitchell]

but we also know that VGE is not the cause of DCS in most people

Really?

So please explain these figures to me.

70% of divers with cerebral DCS had a large PFO compared to 15% of control divers without cerebral DCS.
Germonpre et al. Journal of Applied Physiology 1998;84:1622

75% of divers with spinal DCS had a large PFO compare to 12% of control divers without spinal DCS.
Wilmshurst et al. Clinical Science 2000;99:65

82% of divers with inner ear DCS had a PFO compared to 25% of control divers without inner ear DCS.
Cantais et al. Critical Care Medicine 2003;31:82

...and there are others, but that will do for now.

What you can take from this is that MOST divers suffering these SEVERE DISABLING forms of DCS have a lesion that allows VGE to shunt from the veins to the arteries, and that these findings implicate VGE in causation of these events. Not to mention the essentially irrefutable fact that VGE cause the one form of DCS that can be rapidly fatal (cardiopulmonary DCS).

If you want to know why VGE are common, and these forms of serious forms of DCS are relatively rare, then read:

Mitchell SJ, Doolette DJ. The Pathophysiology of Microbubbles Crossing a PFO or Other Right to Left Shunts in Decompression Sickness. In: Denoble PJ, Holm JR (Editors). Patent Foramen Ovale and Fitness to Dive Consensus Workshop Proceedings. Durham, NC, Divers Alert Network, 43-50, 2016

or

Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: the role of tissue gas supersaturation. J Appl Physiol 106, 298-301, 2009

Finally, stop citing scientists saying that VGE counts cannot be used as a diagnostic tool for DCS as though it somehow supports your fantasy that VGE are pathophysiologically unimportant. ALL of us have ALWAYS made EXACTLY the same observation. The positive predictive value of VGE counts for DCS is poor. That does not mean that they are unimportant. Read the above two references for an explanation.

It is indeed unfortunate that use of your bubble model seems to result in the generation of many bubbles, but that does not give you an excuse to shamelessly misrepresent our knowledge of DCS in order to deflect the legitimate related concerns that people might have.

Simon M

 

[rossh]

Simple facts simon.....

Almost all tech divers (90%+) have VGE, but the frequency of DCS is tiny - 1: 2,500 to 1:10,000.

But as many as 1/3rd of us have some form of PFO or pulmonary bypass or circulation defect of some sort.

So... explain these discrepancies please....

VGE occurrence vs tech injury; 0.9 : 2,500

PFO / pulmonary re-circulations vs tech injury: 1:3 vs 1:2,500


Recreational divers have a VGE rate of about 30%. But an injury rate is 1:10,000. explain that discrepancy please?



All of this leads to the reality: Your colleagues clearly state, VGE is NOT DCS, re: refs post 21 above.


A PFO and Pulmonary bypass, also includes something else you refuse to accept - re-circulation of non-filtered blood, giving reduced gradients and slower off gas rates. That has to be factored into the conditions too (which you refuse to accept, because it diminishes your anti bubble model campaign).

I have no doubt that PFO's has contributing involvement in injury, but your simplistic connection and consequence to VGE, is statistically invalid.

**************

VGE exist is all deco plans and all models and all ascent types. You cannot avoid them. There is 45 years of scuba / deco diving history, ALL of it with VGE involvement. (VGE was first monitored in the early 70's).

Bubble models and deeper stop approaches have been in wide use for 15 years (including all the GF styled emulations), and injury rates are at their lowest in history (from model derived plans). Even with the larger VGE scores typical of deeper stops, we have that lower injury rate..... indicating further that your simplistic VGE injury connection theory is wrong.


****************


Get used to this Simon. Stop trying to invent drama, and shamelessly misrepresent our knowledge of DCS to VGE connection.

All this anti VPM-B voodoo scare tactics campaign of yours are plainly invalid.

.

 

[Simon Mitchell]

Simple facts simon.....

Almost all tech divers (90%+) have VGE, but the frequency of DCS is tiny - 1: 2,500 to 1:10,000.

But as many as 1/3rd of us have some form of PFO or pulmonary bypass or circulation defect of some sort.

So... explain these discrepancies please....

VGE occurrence vs tech injury; 0.9 : 2,500

PFO / pulmonary re-circulations vs tech injury: 1:3 vs 1:2,500

Recreational divers have a VGE rate of about 30%. But an injury rate is 1:10,000. explain that discrepancy please?

As I said in the post above, if you want to know why VGE are common, and these forms of serious forms of DCS are relatively rare, then read:

Mitchell SJ, Doolette DJ. The Pathophysiology of Microbubbles Crossing a PFO or Other Right to Left Shunts in Decompression Sickness. In: Denoble PJ, Holm JR (Editors). Patent Foramen Ovale and Fitness to Dive Consensus Workshop Proceedings. Durham, NC, Divers Alert Network, 43-50, 2016

or

Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: the role of tissue gas supersaturation. J Appl Physiol 106, 298-301, 2009

READ THEM and then come back with your rebuttal if you have one.

All of this leads to the reality: Your colleagues clearly state, VGE is NOT DCS, re: refs post 21 above.

There you go again, citing something we all say as though it supports your argument. The buzz phrase "VGE is not DCS" merely reflects the fact that the positive predictive value of VGE counts for DCS is poor; something everyone agrees on. This does not mean that VGE are unimportant in the pathophysiology of DCS; something only you believe. The most bizarre aspect of this ridiculous argument is that most of the papers / references from which you cherry-pick quotes are actually all about the role of VGE in DCS.

A PFO and Pulmonary bypass, also includes something else you refuse to accept - re-circulation of non-filtered blood, giving reduced gradients and slower off gas rates. That has to be factored into the conditions too (which you refuse to accept, because it diminishes your anti bubble model campaign).

Yes, I refuse to accept it. I have provided you with evidence in the past that the shunt fraction across a PFO is so tiny as to be irrelevant to inert gas exchange. That is why you will not find the issue discussed in any of the many papers and textbook chapters written by many authors on the subject. Why have none of my colleagues ever advocated this as a mechanism by which PFO causes an increased risk of DCS?

I have no doubt that PFO's has contributing involvement in injury, but your simplistic connection and consequence to VGE, is statistically invalid.

Really? So what do YOU propose is the link between PFO and these injuries? I have provided you with a published answer to your questions. How about you provide an answer to mine.....

Please explain these figures to me.

70% of divers with cerebral DCS had a large PFO compared to 15% of control divers without cerebral DCS.
Germonpre et al. Journal of Applied Physiology 1998;84:1622

75% of divers with spinal DCS had a large PFO compare to 12% of control divers without spinal DCS.
Wilmshurst et al. Clinical Science 2000;99:65

82% of divers with inner ear DCS had a PFO compared to 25% of control divers without inner ear DCS.
Cantais et al. Critical Care Medicine 2003;31:82

VGE exist is all deco plans and all models and all ascent types. You cannot avoid them. There is 45 years of scuba / deco diving history, ALL of it with VGE involvement. (VGE was first monitored in the early 70's).

The ubiquitous nature of VGE does not of itself indicate that they are benign. We are constantly surrounded by the bacteria that can cause catastrophic infections as well yet those infections are rare. That does not mean these bacteria don't cause infections.

Bubble models and deeper stop approaches have been in wide use for 15 years (including all the GF styled emulations), and injury rates are at their lowest in history (from model derived plans). Even with the larger VGE scores typical of deeper stops, we have that lower injury rate..... indicating further that your simplistic VGE injury connection theory is wrong.

You have NO idea of the true injury rates in technical diving or during use of deep stop models.

Get used to this Simon. Stop trying to invent drama, and shamelessly misrepresent our knowledge of DCS to VGE connection.

Trust me Ross, I am thoroughly used to your commercially motivated misrepresentation of diving science. My account of the "DCS to VGE connection" is the one that appears in all the diving medicine textbooks and is widely accepted by my colleagues. It is nothing short of comical that you would try to portray it otherwise, and all you are going to achieve here is further confirmation of increasingly widespread perceptions of you.

Simon M

 

[rossh]

Patent Foramen Ovale and Fitness to Dive Consensus Workshop Proceedings, June 17, 2015, Montreal, Canada.

The message that keeps coming up in those papers, is that people with a large PFO, are at much higher risk of injury. They are 2.5 to 5x more likely to get injured, or are likely to have serious injury vs a light one. Even when they dive conservatively, they are still at elevated risk. i.e. (#5) they either need to avoid diving, or get the problem fixed.


There you have it - This group is involved in a higher proportion of all injury treatments. An identifiable highly susceptible sub-group of people that can be pre-tested and take steps to avoid their elevated risk / unprovoked future DCS.


For tech / deco / military / commercial divers, a test would be most beneficial, and would prevent many, many future injuries by isolating / fixing the high risk divers before they get themselves into trouble. I think all future tech divers should get tested, and particularly if they have a spotty history in their recreational days.


But what was the consensus / recommendations of all those papers and discussion?? ..... do nothing.... wait for your first injury and react if its a large PFO,.... fiddle the profiles a bit, and cross your fingers.

That's very sad, and how disappointing. All these medical professionals could have made some solid recommendations to have new tech divers screened, and that would lead to a clear reduction in the future injury rate by half. i.e. test those divers who's diving stress level is more likely of developing an injury. Well worth it at any price I think.

***********

So, now Simon going to tell us to fiddle with profiles (that makes no meaningful risk reduction to the high risk large PFO group anyway). We will be entertained with scare tactics, test numbers blown out of proportion and context, and voodoo implied magical improvements, if only we follow his lead. Simon uses this nonsense approach because its fits into his agenda of anti bubble model campaign.


If you are not in the high risk large PFO group (most of us), then carry on as usual, because VGE have little / no meaningful effect on most of us. Like I said in a previous post..."...VGE is not the cause of DCS in most people....".

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[rjack]

Patent Foramen Ovale and Fitness to Dive Consensus Workshop Proceedings, June 17, 2015, Montreal, Canada.

The message that keeps coming up in those papers, is that people with a large PFO, are at much higher risk of injury. They are 2.5 to 5x more likely to get injured, or are likely to have serious injury vs a light one. Even when they dive conservatively, they are still at elevated risk. i.e. (#5) they either need to avoid diving, or get the problem fixed.


There you have it - This group is involved in a higher proportion of all injury treatments. An identifiable highly susceptible sub-group of people that can be pre-tested and take steps to avoid their elevated risk / unprovoked future DCS.


For tech / deco / military / commercial divers, a test would be most beneficial, and would prevent many, many future injuries by isolating / fixing the high risk divers before they get themselves into trouble. I think all future tech divers should get tested, and particularly if they have a spotty history in their recreational days.


But what was the consensus / recommendations of all those papers and discussion?? ..... do nothing.... wait for your first injury and react if its a large PFO,.... fiddle the profiles a bit, and cross your fingers.

That's very sad, and how disappointing. All these medical professionals could have made some solid recommendations to have new tech divers screened, and that would lead to a clear reduction in the future injury rate by half. i.e. test those divers who's diving stress level is more likely of developing an injury. Well worth it at any price I think.

Since you have it figured out can you point me to your calculations?
How much are current DCS treatment costs across all injuries?
How much do current injury rates cost society in morbidity and mortality?
So how much are the costs to screen everyone?
How many will develop complications from repairs?
What are those costs in morbidity and mortality from complications?

Asking for a friend

 

[Simon Mitchell]

The message that keeps coming up in those papers, is that people with a large PFO, are at much higher risk of injury.

You can't quite bring yourself to say it can you? But let me finish it off.... "almost certainly because a large PFO allows VGE to cross into the arterial circulation".

It is obvious that while VGE numbers cannot be used as a diagnostic tool for DCS (everyone agrees on that), VGE themselves are almost certainly important agents of injury, particularly in the more severe forms of DCS.

There you have it - This group is involved in a higher proportion of all injury treatments. An identifiable highly susceptible sub-group of people that can be pre-tested and take steps to avoid their elevated risk / unprovoked future DCS.....

But what was the consensus / recommendations of all those papers and discussion?? ..... do nothing.... wait for your first injury and react if its a large PFO,.... fiddle the profiles a bit, and cross your fingers.

That's very sad, and how disappointing. All these medical professionals could have made some solid recommendations to have new tech divers screened, and that would lead to a clear reduction in the future injury rate by half.

Well, it is good to know that Ross Hemingway is out here ready to correct decisions by the best minds in diving medicine and protect the diving public from the stupidity of the diving science community. Seriously, have you no insight into your own limitations? Do you really think the expert workshop participants failed to carefully consider this issue?

Mandatory screening would have its own costs, complications, and raise many extremely difficult management decisions (as implied by rjack). And even if we did do what you suggest and exclude or repair every single PFO in the technical diving population, it would still not obviate the need to be worried about VGE as you seem to assume. VGE could still cross a pulmonary shunt and cause exactly the same problems. Pulmonary shunts are potentially present in EVERYONE and there is nothing you can do about them.

The PFO problem can be managed in multiple ways, which includes testing divers where it is indicated, repairing PFOs where it is indicated, and also (as clearly accepted at the workshop) by minimising VGE numbers. Contrary to what you seem to believe, there is evidence that reducing decompression stress reduces the risk associated with a PFO, almost certainly by reducing the numbers of VGE:

Klingmann C et al. Lower risk of decompression sickness after recommendation of conservative decompression practices in divers with and without vascular right to left shunt. Diving Hyperb Med. 2012 Sep;42(3):146-50.

The inescapable conclusion is that all other factors being equal, if you have two decompression profiles of equal length but which distribute their stops differently, and one produces more VGE than the other, then you would choose the one that produces less VGE. To try to argue against this fundamental principle is ridiculous.

Simon M

 

[rossh]

Since you have it figured out can you point me to your calculations?
How much are current DCS treatment costs across all injuries?
How much do current injury rates cost society in morbidity and mortality?
So how much are the costs to screen everyone?
How many will develop complications from repairs?
What are those costs in morbidity and mortality from complications?

Asking for a friend

Your putting it into dollar terms.... That's not what is important here. Its about avoiding an injury that is predictable.

Clearly they have found and shown an easily identifiable medical condition that causes / contributes highly to injury. If you are one of those unlucky few, your about 5x times more likely to get injured, even when doing your diving perfectly well, and conservatively.

These people cannot mange this by fiddling the plan - you cannot make your plan 5x more safer to compensate for the large PFO.

I agree its not worth testing the general recreational diver, but tech divers are a very small subset of diving, and we are engaging in the more dangerous end of this sport. It defiantly has benefits to find and eliminate the problem divers, before they get themselves injured.

If we eliminated / fixed the worst and most injury prone people before they got bent, then its a win for them, and us. Doing this would cut the overall future injury rate in about half for the tech divers.


What's the negative side? It costs the new tech diver a medical test expense. The few who turn out to have the large PFO will face a decision.... avoid all tech diving, get it fixed, or know with certainty to get bent in the future and all the pain, risk and residual medical problems that involves.


How is this different to other health screening? People get routine medical checks for the onset of all kind's of disease and ailments - diabetes, heart health, prostate, cancers, etc. We do this to avoid / rectify / limit bigger problems later in life. DCS is a very serious condition... why can't we pre-test for that too?


******

How much would you pay / sacrifice to know that your conservative planning and dive technique, has been undermined and rendered noneffective, because your body has a defect that will cause you to get bent today?


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