Diving too carefully?

[npollock]

Michael,

"Symptomatic DCS" is close to a redundant term since symptoms must exist for the label "DCS" to be applied. I say close, because in conversation (or writing) it could be used to distinguish frank symptoms from "subclinical DCS." Conceptually, the latter describes a condition in which symptoms are not manifest but it is felt that there is enough decompression stress to warrant acknowledgment. This may or may not develop into DCS but part of the subtext is the open question as to whether pushing this range could have negative ramifications in the long run. Low grade "niggles" are minor, frequently transient symptoms that can wax and wane (progress and dwindle) over a short period of time. Again, it is unclear if these have any long term ramifications but the conservative recommendation would be to try and avoid conditions in which any symptoms - major, minor or transient - develop.

Clinical diagnosis involves medical art and judgment. The decision to treat is often biased towards the conservative 'when in doubt, treat,' which is a welcome position for an afflicted individual. The ultimate classification of individual cases is more complex. One effort to evaluate expert opinion is found in a paper described in the following abstract:

Freiberger JJ1, Lyman SJ, Denoble PJ, Pieper CF, Vann RD. Consensus factors used by experts in the diagnosis of decompression illness. Aviat Space Environ Med. 2004 Dec;75(12):1023-8.
INTRODUCTION: The diagnosis of decompression illness (DCI) is entirely based on clinical findings and DCI experts are rare. Of all the chambers reporting to Diver's Alert Network (DAN), 86% see less than 10 cases per year. Simulated diving injury cases (vignettes) were used to identify diagnostic factors important to 11 international experts attending the 2003 Undersea and Hyperbaric Medical Society symposium on DCI diagnosis. METHODS: There were 200 vignettes evaluated for the probability of DCS and/or arterial gas embolism (AGE). Vignettes were constructed from 141 factors that modeled information from DAN's emergency call system. Factor probability mirrored DAN's 2001 Report on Decompression Illness and Diving Fatalities. Factors included: diver characteristics, exposure characteristics, signs, symptoms, treatment, and response. Multiple linear regression with stepwise elimination identified and ordered the significant factors in terms of their importance to the experts. Results were confirmed with logistic regression. RESULTS: For DCS, the top five factors in order of importance were: 1) a neurological symptom as the primary presenting symptom; 2) onset time of symptoms; 3) joint pain as a presenting symptom; 4) any relief after recompression treatment; and 5) the maximum depth of the last dive. For AGE, the top five factors were: 1) onset time of symptoms; 2) altered consciousness; 3) any neurological symptoms as a presenting symptom; 4) motor weakness; and 5) seizure as the primary presenting symptom. Age, gender, or physical characteristics were not statistically important. CONCLUSIONS: The vignette concept may be useful in the development of consensus standards for DCI diagnosis.


Definitions are frequently established in advance for scientific evaluation of individual cases. It is possible that a case would not reach the threshold for scientific classification as DCS even with a clinical diagnosis. Again, this bias towards treatment is good for the patient. The more rigorous determination for scientific study is part of the effort to get a handle on some of the variability. We recently published an attempt at scientific review of cases involving scientific diving that were reported to the American Academy of Underwater Sciences. I do not hold this out as the best example - the records were very thin in a number of cases - but it is an example of how the scientific effort can be separated from the clinical determination. The abstract follows:

Dardeau MR, Pollock NW, McDonald CM, Lang MA. The incidence of decompression illness in 10 years of scientific diving. Diving Hyperb Med. 2012 Dec;42(4):195-200.
BACKGROUND: The American Academy of Underwater Science (AAUS) constitutes the single largest pool of organizations with scientific diving programmes in North America. Members submit annual summaries of diving activity and any related incidents. METHODS: All diving records for a 10-year period between January 1998 and December 2007 were reviewed. Incidents were independently classified or reclassified by a four-person panel with expertise in scientific diving and diving safety using a previously published protocol. Subsequent panel discussion produced a single consensus classification of each case. RESULTS: A total of 95 confirmed incidents were reported in conjunction with 1,019,159 scientific dives, yielding an overall incidence of 0.93/10,000 person-dives. A total of 33 cases were determined to involve decompression illness (DCI), encompassing both decompression sickness and air embolism. The incidence of DCI was 0.324/10,000 person-dives, substantially lower than the rates of 0.9-35.3/10,000 published for recreational, instructional/guided, commercial and/or military diving. CONCLUSIONS: Scientific diving safety may be facilitated by a combination of relatively high levels of training and oversight, the predominance of shallow, no-decompression diving and, possibly, low pressure to complete dives under less than optimal circumstances.


There are no diagnostic tests that establish the presence (or absence) of DCS. A substantial amount of effort is directed at identifying biomarkers of DCS. I mentioned some of the work involving microparticles earlier. While microparticle counts do rise with decompression stress (and other stressors) the substantial variability make it unlikely that a diagnostic test will be coming soon. The hunt continues. In the meantime, confidence in the diagnosis of DCS certainly does rise when symptoms respond in an expected manner to therapeutic treatment.

 

[rossh]

The only person I've seen arguing that they are different is you. Intramuscular or in any other tissue but blood is bad. But paradoxically, in venous blood, you appear to say they are a good thing. I say apparent position because its not always clear to me. Citing one rather old text (which doesn't actually present any primary data) is not very convincing evidence of this position honestly.

Drs Mitchell and Pollack have been much clearer about the desirability of VGE (less is better but below grade 2 is not measurably better than none). Personally I am not diving in a way to try to 'optimize' my VGE just below some fuzzy symptomatic threshold. In part because even in one subject (me) that threshold is wide, gray, and not static. I want to be on the conservative end/side of the gray zone, whereas some of the bubble models and BSAC tables sure seem to be more towards the aggressive side of the gray swath between ridiculous amounts of decompression and clinically bent.

Obviously there is a point where I would consider myself "too conservative", but adding ~10% to my deco time to conduct extended shallow stops and potentially reduce my VGE from >2 to <2 is not "too conservative" for me. The exception would be when some other issue is concurrent and I need to make a risk management decision e.g. freezing due to a suit flood, running out of deco gas.

Hi,

You are closing the barn door, after the horse has bolted.

The world has been diving blind to its VGE numbers. Divers has been doing just fine so far. Deco models we use today is pretty conservative all around, compared to what was available 20 years ago. But now that a VGE numbers are getting wider attention, you want to make new slower limits? It's all very hypocritical. What worked before still works, and trying to say some new arbitrary VGE number is now unacceptable, is not being honest with yourself or the reality.

You are welcome to go slower and safer if you feel the need - you learn this basic principle in scuba class - to make it safer - extend the time, and the VGE is simply a confirmation of that. But please do not imagine for one second, that the existing practices are bad, as the proof is in the pudding already.

 

[rossh]

Ross, I have not seen Simon post anywhere in this thread that bubble models are at fault. Let's not unnecessarily stir the pot. Let's please try to keep the discussion on track and avoid trying to read between the lines.

Hi Randy. Do you read every post in this forum? I guess not. Where were you when I report the insulting and and derogatory posts Simon made about me?


PS: We didn't need to wait long. Simon launches into his bubble models are bad routine in just 5 posts below. #348

 

[Simon Mitchell]

Ross,

You are attempting to reframe the debate into one about using VGE to investigate / modify decompression strategies. I am happy to have that discussion, but I wish to remind you that the original issue has always been your insistence that VGE don't cause DCS and can be ignored. I am confident that sufficient information has been presented in this thread for readers to come to the correct conclusions on that question.

In respect of the points you raise about VGE as an end point for decompression investigation / profile selection:

Divers has been doing just fine so far.

Except the ones that I, and my many local and international colleagues have treated in our hyperbaric units.

What worked before still works, and trying to say some new arbitrary VGE number is now unacceptable, is not being honest with yourself or the reality.

Except that the concept of using VGE to evaluate decompression protocols is neither "new" nor "arbitrary".

Its not "arbitrary" because, as pointed out to you many times, there are solid data linking higher DCS risk to higher VGE grades.

Its not "new" because, as pointed out to you many times, various groups have been basing decompression profile testing on VGE measurement for decades.... including the DCIEM whose test program you have praised in the past.

Given the relationship between high VGE grades and DCS surely it is sensible to investigate the optimal means of consistently avoiding high bubble grades during decompression? As Neal has pointed out, this does not mean striving for no VGE because there is little statistical relationship between low grades and DCS. And nor does the aim of avoiding high grades necessarily mean endlessly longer decompressions. As you well know, NEDU have published evidence that different patterns of decompression can produce different bubble grades, even when the decompressions are of equal length. I'm not going to get into that here, but surely this sort of research (which is sort of what Neal is doing in an informal way with his field studies) has merit?

To be honest, given that you produce decompression software I think it is disappointing that you seem dismissive of attempts to improve safety through decompression research that uses the most readily acceptable outcome measure currently available. Aren't you interested in identifying decompression strategies / patterns that might consistently lower the incidence of a state (high VGE) which is associated with higher DCS risk?

But please do not imagine for one second, that the existing practices are bad, as the proof is in the pudding already.

You could only justify this statement if: A. you could cite an accurate incidence of DCS in technical diving, and that would require a large prospectively gathered database of dives of known outcome; and B. there was a consensus among experts that the DCS incidence measured from this database was so low that it was not worth pursuing further research to improve things.

I know you have neither.

Simon M

 

[rossh]

Ross,

You missed one important element in your review of the four abstracts I included. The Swan et al. paper from Jay Buckey's group looked at both intravascular and extravascular bubbles. What they found was that the dual frequency ultrasound systems allowed them to see signals for very small (the size was not measured but indicated by the ultrasound frequency used) extravascular bubbles before they saw the larger intravascular bubbles. This work actually reinforces the common nature of bubble formation. The tool is being developed so we do not have to rely solely on intravascular bubbles to assess real-time decompression stress. This was the unit that I said we have used with a limited number of human trials in our lab. The technology is coming. Most important to this discussion, it is reinforcing the points I tried to make about how different tissues can lead or lag behind another tissue, but that the physical laws remain constant throughout different tissues.

The Bennett and Elliott chapter does not state that the process of bubble formation is fundamentally different in different tissues, and the best evidence we have also supports a fairly consistent formation process. I think it is time for a new question.

Hi Neal,

Thanks for that.

I am not implying a fundamental difference. I don't know where you got that sense from.

I would expect that both locations of micro-bubble, to grow for all the same physical reasons and conditions. But I would also expect each to form at a different time, under different conditions, and different rates and end sizes, with different lifetimes.

It's for all these reasons, and the information you provide above, that I think we need to keep addressing the microbubble sources separately.


******


"... to see signals for very small ... extravascular bubbles before they saw the larger intravascular bubbles.. "


Yes, I think that is just what one would expect. Dissolved gas in tissue initially form and grows micro-bubbles (extravascular), then as the off gassing and the ascent progresses, and dissolved gas enters the circulation again, its made available to grow into VGE (intravascular).


**********


For bubble models, this is exciting news. The central theory of a bubble model is that micro-bubbles will form and exist in tissue (extravascular) for almost every dive, and these can be controlled to an acceptable dimension though ascent limits.

It's satisfying to hear that the micro-bubble theory and research that started in the 70's, is coming to life with advanced detection tools available today.

 

[rossh]

Ross,

You are attempting to reframe the debate into one about using VGE to investigate / modify decompression strategies. I am happy to have that discussion, but I wish to remind you that the original issue has always been your insistence that VGE don't cause DCS and can be ignored. I am confident that sufficient information has been presented in this thread for readers to come to the correct conclusions on that question.

In respect of the points you raise about VGE as an end point for decompression investigation / profile selection:



Except the ones that I, and my many local and international colleagues have treated in our hyperbaric units.



Except that the concept of using VGE to evaluate decompression protocols is neither "new" nor "arbitrary".

Its not "arbitrary" because, as pointed out to you many times, there are solid data linking higher DCS risk to higher VGE grades.

Its not "new" because, as pointed out to you many times, various groups have been basing decompression profile testing on VGE measurement for decades.... including the DCIEM whose test program you have praised in the past.

Given the relationship between high VGE grades and DCS surely it is sensible to investigate the optimal means of consistently avoiding high bubble grades during decompression? As Neal has pointed out, this does not mean striving for no VGE because there is little statistical relationship between low grades and DCS. And nor does the aim of avoiding high grades necessarily mean endlessly longer decompressions. As you well know, NEDU have published evidence that different patterns of decompression can produce different bubble grades, even when the decompressions are of equal length. I'm not going to get into that here, but surely this sort of research (which is sort of what Neal is doing in an informal way with his field studies) has merit?

To be honest, given that you produce decompression software I think it is disappointing that you seem dismissive of attempts to improve safety through decompression research that uses the most readily acceptable outcome measure currently available. Aren't you interested in identifying decompression strategies / patterns that might consistently lower the incidence of a state (high VGE) which is associated with higher DCS risk?



You could only justify this statement if: A. you could cite an accurate incidence of DCS in technical diving, and that would require a large prospectively gathered database of dives of known outcome; and B. there was a consensus among experts that the DCS incidence measured from this database was so low that it was not worth pursuing further research to improve things.

I know you have neither.

Simon M

Yes Simon, I can see the sky is falling over here too .... run for the hills.

 

[Simon Mitchell]

Neal, Simon, Ross I was wondering if I could get some simple definitions of a few terms:
DCS vs Symptomatic DCS. How are you deciding to use one term vs the other? If bubble presence or pressure related stress does not necessarily equal DCS but symptoms do at what point do you call it or consider it DCS? (Is it always the same definition for all of your research)

I thought I had been told that successful treatment is how you can diagnose as DCS with the most confidence. If someone is not treated what methods are you using to diagnose as DCS especially if they lived and/or no autopsy was performed?

Hello Michael,

Neal has done a great job of addressing this. I will add a few comments.

DCS is a clinical diagnosis... that is to say that the doctor must make the call. As Neal pointed out, there are no tests (eg a blood test) that allow you to say, "yes you have DCS" or "no you don't".

The more serious cases are the easiest for obvious reasons. A diver who develops weakness in both legs soon after surfacing from a decompression dive almost certainly has spinal DCS. Very occasionally there can be confusion with other diagnoses like a stroke occurring in temporal relation with a dive, but such cases are vanishingly rare.

The mild cases are the most tricky and I think this is the end of the spectrum you are most interested in. One of the problems is that many of the symptoms of mild DCS are what we call "non-specific", that is, they could be caused by many things. For example, musculoskeletal pain, fatigue, headache, rash are all symptoms of DCS but they can all be caused by many other problems, some of which are highly relevant to the diving environment. Diagnosing a diver presenting with these sorts of non-specific symptoms is a difficult nuanced process in which the doctor must bring together a knowledge of diving, decompression, DCS, and general medicine. Many factors can influence the interpretation, such as (in no particular order): the nature of the dive profile, the presence of risk factors for DCS (cold, hard working dive), the nature of the symptoms, the temporal relation of symptoms with diving, the identification of plausible alternative explanations for the symptoms, the response to oxygen (but see in relation to HBO below), the diver's medical history including past history of DCS, the findings of a physical examination and other things. I could spend a lot of time discussing this. Anyway, all of this gets integrated and you have to make a call. The difficulty with such calls, and the profound implications they can have if, for example, the diver is in a remote location, make taking diving emergency calls quite stressful at times.

Out of a desire to do the right thing by divers diving physicians tend to have a reasonably low threshold for making the diagnosis and recompressing the diver. This inevitably means that some divers who probably don't have DCS do get recompressed from time to time. I am aware of the perception that the response to hyperbaric oxygen (HBO) helps validate the diagnosis, but most of us are cautious about such interpretations. I have seen divers walk into a chamber with relatively mild symptoms and emerge paralysed after a maximally extended Table 6. Thus, some forms of DCS can get worse despite recompression (though this is rare). Equally, some symptoms not due to DCS might well respond to HBO, either because of a placebo effect or a real pharmacological effect of the HBO.

The difficulty with diagnosing mild or equivocal cases, especially where the diagnosis might have profound logistic implications led to the convening of the UHMS Remote DCS Workshop in Sydney in 2004. Up to that time the received wisdom was that once a diagnosis of DCS was made, it was more or less obligatory for the diver to be recompressed. This might mean evacuating someone from a very remote location at enormous expense for (for example) elbow pain that could be DCS or could be due to lifting tanks. The workshop came to a landmark consensus in developing a case definition of "mild DCS" and agreeing that cases that met that definition could be adequately treated with DCS first aid measures (which obviously include surface oxygen). The consensus is over 10 years old now, and has been invoked many times. It appears robust. I would be happy to provide anyone interested in the case definition of "mild DCS with a copy of the proceedings.

MITCHELL SJ, DOOLETTE DJ, WACHHOLZ C, VANN RD (eds). Management of Mild or Marginal Decompression Illness in Remote Locations – Workshop Proceedings. Washington DC, Undersea and Hyperbaric Medical Society, 240pp (ISBN 0 9673066 6 3), 2005

Finally, on the subject of case definitions, your question regarding research is very pertinent. It is one of the great worries in conducting DCS research that your study population gets contaminated by subjects with mild non-specific symptoms who don't actually have DCS. One option is to develop a case definition that focuses on the more specific symptoms, or the more serious ones. But this has the potential to limit your numbers considerably. Another approach, often used in the NEDU studies, is to say it is DCS if an experienced DMO makes the diagnosis and decides to recompress the diver.

I hope this helps answer your questions.

Simon M

 

[Simon Mitchell]

Dissolved gas in tissue initially form and grows micro-bubbles (extravascular, then as the off gassing in ascent progresses and dissolved gas enters the circulation again, its made available to grow into VGE (intravascular).

For bubble models, this is exciting news. The central theory of a bubble model is that micro-bubbles will form and exist in tissue (extravascular) for almost every dive, and these can be controlled to an acceptable dimension though ascent limits.

There are several substantial flaws in this argument. If bubble models produce more high grade VGE than another approach, then it is virtually impossible that they would concomitantly be doing a better job (than the other approach) of controlling bubble formation in a tissue just a couple of microns away from where those high grade VGE are forming from the same supersaturated gas in the capillary blood.

In addition, if bubble models produce more VGE and VGE themselves are responsible for some of the most important forms of DCS (by crossing a PFO etc as discussed extensively above) then, well, I think you can see what I am getting at.

Simon M

 

[rossh]

There are several substantial flaws in this argument. If bubble models produce more high grade VGE than another approach, then it is virtually impossible that they would concomitantly be doing a better job (than the other approach) of controlling bubble formation in a tissue just a couple of microns away from where those high grade VGE are forming from the same supersaturated gas in the capillary blood.

In addition, if bubble models produce more VGE and VGE themselves are responsible for some of the most important forms of DCS (by crossing a PFO etc as discussed extensively above) then, well, I think you can see what I am getting at.

Simon M

Well that's a silly argument.

Shallow stops profiles will likely make more extravascular micro-bubbles, due to higher supersaturation pressures, and that's where neurological DCS is thought to occur.

And shallow stops make VGE too. But high VGE is a surface event mostly, where the supersaturation pressures are all about same for any plan method you might choose.

But of course its all a lot of guess work here, because we have no details of any interaction between extravasular and intravascular conditions in this study.


All deco models are concerned first and foremost, with extravascular micro-bubble tissue growth only, and the dissolved gas formula and supersaturation limits that controls this, because this is where the neurological DCS is thought to occur.

Do I need to remind you - VGE presents a danger to those who have a defective circulation, and those people cannot tolerate VGE - meaning they should keep away from high stress diving practices.


Your persistent efforts to demonize VGE is getting a little ridiculous.

 

[fibre]

Ross,

Ive read through 35 pages of arguments, presenting various arguments for and against VGE as being bad but how can you accuse someone of demonizing VGE when another scientist, you say you respect, states;

High intravascular bubble grades have a stronger association than lower grades, and a much, much stronger association than zero grade VGE.

VGE can clearly cause direct harm

I think both statements are fairly clear and unambiguous.

 

[Igor P]

There are several substantial flaws in this argument. If bubble models produce more high grade VGE than another approach, then it is virtually impossible that they would concomitantly be doing a better job (than the other approach) of controlling bubble formation in a tissue just a couple of microns away from where those high grade VGE are forming from the same supersaturated gas in the capillary blood.

In addition, if bubble models produce more VGE and VGE themselves are responsible for some of the most important forms of DCS (by crossing a PFO etc as discussed extensively above) then, well, I think you can see what I am getting at.

Simon M

Hi Simon,

I think your are misquoting Ross. He did not say a word about bubble models doing better or not better job, but talked about central idea behind bubble models in quoted comment.

You are talking about different aproaches on decompression what is not subject of this thread (I belive) or his comment.

I can agree with Ross, I am excited too on new developements of tools that are able to measure bubble dimensions. Not just counting, but measure actual diameter of bubbles and diferentiate them. I think they will clear lot of things we do not know jet, but only imagine - conclude based on some suppositions how they are. I hope lot of questions can be answered when they are available.

Igor P

Sent from my PAP4500DUO using Tapatalk 2

 

[rossh]

Ross,

High intravascular bubble grades have a stronger association than lower grades, and a much, much stronger association than zero grade VGE.

VGE can clearly cause direct harm

Ive read through 35 pages of arguments, presenting various arguments for and against VGE as being bad but how can you accuse someone of demonizing VGE when another scientist, you say you respect, states;

I think both statements are fairly clear and unambiguous.

Do we need to restate the conditions and qualifiers for those statements?

1/ No one goes to the chamber because they have VGE. There has to be other events, or failures and influences to occur. That is why the predictive correlation is a weak 4% only.
2/ Sure, but you will need to a/ abuse the procedure, or b/ have defective circulation, or c/ have other health issues, and more.

 

[Igor P]

Neal,

Thank's for answers.... they clear some questions I had.

Thank you!
Igor P

Sent from my PAP4500DUO using Tapatalk 2

 

[rjack]

The world has been diving blind to its VGE numbers. Divers has been doing just fine so far. Deco models we use today is pretty conservative all around, compared to what was available 20 years ago. But now that a VGE numbers are getting wider attention, you want to make new slower limits? It's all very hypocritical. What worked before still works, and trying to say some new arbitrary VGE number is now unacceptable, is not being honest with yourself or the reality.

Well nobody really knows how many divers got bent on a BSAC table do we? (or most other tables for that matter)

So VGE aren't a worthwhile tool for looking at the magnitude of decompression stress in your mind. What is the right tool? Seems like you are saying we shouldn't bother trying (to measure and figure out practices to reduce VGE) if people aren't clinically bent everything must be A-ok.

I know there are some non-bubble markers of decompression stress out there and Neal has mentioned a few. What should be used and why?

 

[Michael Thornton]

Hello Michael,

Neal has done a great job of addressing this. I will add a few comments.



I hope this helps answer your questions.

Simon M

Thank you Neal and Simon very informative. Simon I would love a copy of the proceedings. Diagnosing, dealing with, and preventing DCS in remote locations is probably one of my biggest interests right now.

 

[npollock]

Practices frequently change as understanding evolves. Not many people coat themselves with baby oil to sunbathe anymore. Diving is no different and we do know more now than we once did.

I believe that dysbaric osteonecrosis (DON) was mentioned early in this thread. If I recall correctly, it was quickly turned aside as being a problem for "commercial divers." There was a dedicated effort to study commercial divers in the 60s and 70s after a high frequency of DON were discovered. Decompression procedures were altered and the frequency declined in the community. The important thing to appreciate, though, is the risk factors found to be associated with increased risk. There were two: a history of diving to depths greater than 50 m (165 ft) and a history of inadequate or experimental decompression. Fast forward to our current reality. You no longer have to be a commercial diver to regular exceed 50 m or develop a history of experimental if not inadequate decompression. All you need to be is a technical diver.

One of the major reasons I promote conservative practice is that avoiding acute symptoms of DCS addresses only the first hurdle. Like sunbathing, the price for incautious practice may be paid years down the road. Minimizing bubble loads may well be important to ensuring that we do not see a resurgence of DON in the next 10 to 20 years.

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.

Blaming "defective circulation" for decompression problems is not credible based on the research evidence we have in hand. As has been discussed, bubbles cross a healthy pulmonary bed at an increasing rate as exercise intensity increases. The best way to avoid bubble problems is to limit their formation - in any tissue. Adding reasonable conservatism can reduce the risk for acute or chronic issues. I like to employ the "loved one" rule. Is the practice I promote one that I would welcome for a loved one? Everyone should evaluate sources of information critically and then decide on their risk tolerance. The biggest disservice that I see is when someone with a high risk tolerance encourages others to explore the edges when they do not share the same tolerance.

I see the best community leadership in encouragement of thoughtful practice that favors a long and injury-free diving life. Getting out of the water fast is a trivial benefit in comparison. We do not have all the answers, but we know enough to appreciate the value of safety buffers, even if they exceed what we have gotten away with in the past.

Healthy diving.

 

[GLOC]

Michael, Rubicon is your friend http://archive.rubicon-foundation.org/xmlui/handle/123456789/5523

 

[cys]

Do we need to restate the conditions and qualifiers for those statements?

1/ No one goes to the chamber because they have VGE. There has to be other events, or failures and influences to occur. That is why the predictive correlation is a weak 4% only.
2/ Sure, but you will need to a/ abuse the procedure, or b/ have defective circulation, or c/ have other health issues, and more.

The Sisyphean ball has just rolled back to its starting point.

 

[Simon Mitchell]

Shallow stops profiles will likely make more extravascular micro-bubbles, due to higher supersaturation pressures, and that's where neurological DCS is thought to occur.

You have no basis for your claim that shallow stop profiles will make more extravascular bubbles; indeed, the only studies comparing bubble formation after deep or shallow stop decompression dives show that bubble models produce more VGE (which is why your campaign to discount the importance of VGE started). For the reasons outlined in my earlier posts, it is implausible that bubble models could control extravascular bubbles better than another approach while at the same time producing higher numbers of VGE.

And as I have pointed out to you many times, and as you will find throughout the diving medicine literature, neurological DCS can be produced by intra- or extravascular bubbles. Indeed, the overwhelming weight of evidence favours intravascular bubbles for brain and inner ear, with more of a balance for spinal. If you can find any data that indicates otherwise, please present it.

All deco models are concerned first and foremost, with extravascular micro-bubble tissue growth only, and the dissolved gas formula and supersaturation limits that controls this, because this is where the neurological DCS is thought to occur.

All deco models are concerned first and foremost with preventing symptoms of DCS. Go and look at your copy of Bennett and Elliott, in Bill Hamilton and Ed Thalmann's chapter on "Decompression Practice", after mentioning both intravascular and extravascular bubbles, they clearly state:

"At any rate, no matter what the ultimate cause, the object of designing a proper decompression procedure is to avoid DCS; whether or not this involves avoiding bubble formation altogether or by keeping the bubble formation at or below a tolerable level is still a subject for debate"

And once again, with your claim that neurological DCS is thought to occur through extravascular bubble formation, you unilaterally rewrite the pathophysiological wisdom of the entire field to suit your narrative. This is simply wrong. This is NOT what the literature says. Go and read widely, and if you can find evidence to support your claim, please present it.

Do I need to remind you - VGE presents a danger to those who have a defective circulation, and those people cannot tolerate VGE - meaning they should keep away from high stress diving practices.

I trust you have seen Neal's comment.

Blaming "defective circulation" for decompression problems is not credible based on the research evidence we have in hand.

Your persistent efforts to demonize VGE is getting a little ridiculous.

Please see fibre's post in which he points out that Neal and I agree on this:

http://www.ccrexplorers.com/showthread.php?t=18348&p=178436&viewfull=1#post178436

In fact, my "persistent effort" is to prevent you from contaminating a knowledge base that has taken decades of hard work to accumulate with grossly incorrect information, but as CYS has observed, when someone is as determined as you are, it all becomes a bit interminable and pointless.

Simon M

 

[Simon Mitchell]

2/ Sure, but you will need to a/ abuse the procedure, or b/ have defective circulation, or c/ have other health issues, and more.

Which one of these applied to Neal's 4 cases of cardiopulmonary DCS?

VGE can clearly cause direct harm. This thread has already contained discussion of cardiopulmonary symptoms ("chokes") associated with intravascular bubble loads that are high enough to overwhelm the lungs filtration ability and impair effective gas exchange. This has been well demonstrated in animal studies, and we have had four cases in our lab. One of these was beautifully captured in one of our NASA studies. Very high bubble loads preceding the onset of mild but escalating symptoms of coughing, retrosternal pain, and anxiety. Rapid descent brought rapid resolution of the symptoms; it could very well have been a life-threatening situation had the fast action not been taken.