Diving too carefully?

[Simon Mitchell]

Once again we see you Simon taking every opportunity to make attacks against me... because I dare to stand up to his egotistical arrogance and fallacies.

Ross,

As long as you continue to post incorrect material relevant to my areas of interest I will continue to correct you. Many readers of these forums are serious about acquiring accurate information / knowledge and because of your association with VPM some may assume you know what you are talking about in matters beyond your area of undoubted expertise (software interfaces for decompression algorithms). If you don't want any more "attacks" then refrain from authoritative commentary on matters that you know very little about.

The scientifically accepted source of VGE is what I briefly described - they are thought form on the venous endothelium from passing supersaturated venous blood. That's what the Bennett and Elliotts' Physiology and Medicine of Diving, book is saying.

I wrote the chapter on pathophysiology of DCS in Bennett and Elliott. I'm well aware of the fact that one theory of venous bubble formation has them forming on the endothelium in tissue capillaries. The point you keep dancing around is where the venous blood acquires supersaturated gas; the answer, of course, being "the tissues". Thus, the propensity for bubble formation in the venous blood is inextricably linked to the supersaturation of the tissues through which the blood is passing. You have tried to deny / downplay this in numerous posts in numerous threads.

But I sense you want to change that concept to suit your new "VGE is bad" paradigm.

It is neither mine nor new. Numerous authors have correlated risk of DCS with numbers of VGE over many years of research. The correlations are certainly not adequate to use VGE to diagnose DCS, but there is no denying that higher VGE grades are associated with a higher risk of DCS. Similarly, DCS virtually never occurs in the absence of VGE. In addition, the only plausible reason a PFO can be linked to cerebral, spinal, inner ear and cutaneous DCS (as has been established by many studies) is that the PFO allows VGE to enter the arterial circulation and distribute to these organs. So, VGE are implicated in causation of some of the most serious forms of DCS (via a PFO) and while we all understand that VGE are common and some exposure can be tolerated without symptoms, they are also bad.

A person "with a large PFO", is going to have all kinds of deco issues, and should not be doing high risk dives at all, and most likely have a long history of troubles.

There are many instances of divers going for years without problem, then suffering DCS and having a large PFO discovered.

Further, your theory fails given the following study:
J Appl Physiol (1985). 2013 Sep 1;115(5):716-22. doi: 10.1152/japplphysiol.00029.2013. Epub 2013 Jun 13.
Exercise after SCUBA diving increases the incidence of arterial gas embolism. Madden D1, Lozo M, Dujic Z, Ljubkovic M.
Here they found more than half of the subjects created AGE, just from post dive exercise (they were all non PFO people). So one might assume if half of us can have AGE from shore diving and climbing the ladder, your vision cause theory would be common place in diving. But i don't think it is.

Its not my vision theory. Visual manifestations after exposure to arterial emboli are a well-recognised medical phenomenon, and visual changes have been a recognized symptom of DCS for as long as the disease has been known. Most importantly, you cite (from Madden's paper) a proportion of subjects who exhibited right to left shunting of bubbles via pulmonary shunts after diving, but not the number of bubbles shunted. A big PFO is much more likely to allow a large shower of VGE to cross into the arteries after a valsalva than pulmonary shunts, and so symptoms are therefore more likely in that context. Nevertheless, I have no doubt that pulmonary shunts are contributory in at least some cases.

Simon M

 

[rossh]

No Ross he doesn't make anything up, he merely read what GLOC had written more closely than you (which is the same thing as saying he actually bothered to read it).

"However, when I got back to the UK I had a PFO test with Dr Mark Turner and found that I had an 8mm x 12mm PFO which has been subsequently fixed with an Amplaster device. As part of my RAF medical I had to see the medical board and the only thing the President of the board, one of the world leading doctors on high altitude rapid decompression, could think of was excessive bubbling in the eye as there were no other symptoms, but seeing as that is nigh on impossible to test in lab conditions following dives, then there is limited evidence to prove one way or another.

That was his G's follow up post. My comment that was to his initial post, and is perfectly correct.

Now you should write to G and ask him to discuss this, as I have done...... There is no DCS in this. I won't reveal what he said, but maybe he will share it with you privately.

 

[silentbob]

That was his G's follow up post. My comment that was to his initial post, and is perfectly correct.

Now you should write to G and ask him to discuss this, as I have done...... There is no DCS in this. I won't reveal what he said, but maybe he will share it with you privately.

So you have a secret, one that can't be revealed publicly, but that at the same time you rely on in your argumentation. An argumentum sub rosa?

How convenient for you, and how obscurantist of you to behave in this manner.

 

[rossh]

So you have a secret, one that can't be revealed publicly, but that at the same time you rely on in your argumentation. An argumentum sub rosa?

How convenient for you, and how obscurantist of you to behave in this manner.

It is his medical issue. I respect his privacy. Your insults and allegations directed at me are not appropriate.

 

[silentbob]

Then don't include it in your discussion if you're so respectful of his privacy!

You said "I also had a private conversation with G on this matter,..." you wrote that in an attempt to insinuate that you were correct due to information you could not disclose. In doing so you disclosed (if you're to be believed) to everyone that he has a medical issue that caused his symptoms that was unrelated to his now fixed PFO.

Your method of conducting yourself on this forum is what is not appropriate Ross.

You repeatedly conduct yourself in the manner of a charlatan.

 

[Mark Chase]

Hi Mark,

That holy grail you seek, does not exist.

True but we have to work with what we have got in the moment. I have radicly altered my deco many times in serch of it. IE No deep stops on IANTD tables to GF deco 10/80 and 3m/min ascents, Ignoring He in the mix, GF Deco 70/85GF ASAP to first stop depth

I am still trying to find it bassed on best available info

Remember we are forcing high pressure gas into tissue and bone, and letting it out again slowly, in a way that has never been part of our human evolution. Fiddling the deco a little this way or that way, is not likely to change the long term outcome.

Ish

Yes i am sure all deco is bad and all dives are deco dives right so all diveing is bad, but I feel that agressive deco does long term dammage thats not yet recovered in time for the next dive and therefore becoms a compound problem.

But i stress its a personaly held beleife and I have no medical trainig past 02 admin

Our bodies age - we get old sore and slow, and have reduced physical abilities. Diving is a physiological activity. Why do you think that divers should be excused/absolved of that process?

Yes but some of the bent / PFO divers i am talking about are young and very fit

I am a fat old drunken ex full time smoker who still smokes ocasionaly and I have never knowingly been bent post dive.

BUT I have always erred on the side of what I felt was conservitive deco

60/90 probably being the most agressive i have run

on 70/85now

Go figure

 

[Mark Chase]

There are many instances of divers going for years without problem, then suffering DCS and having a large PFO discovered.

Simon M

Thats the bit I cant get my head arround

Is cumlative dammage a possable reasion or an i just talking out of my oversized arse again

ATB

Mark

 

[Ben Field]

Thats the bit I cant get my head arround

Is cumlative dammage a possable reasion or an i just talking out of my oversized arse again

They are just lucky/statistically unfortunate due to flying inside the curve for much of the time- (trying desperately to steer the thread back on course ;-)

I have met the "I got bent, been diving the same way 20years and nothing then this!" type of disbelieving divers and on questioning you discover a perfect storm- cautious diving for 20years but now older, dehydrated from a few beers the night before, didn't sleep due to other snoring divers on trip, slight current, hard work with the DSMB reel and wham-bang= first bend on innocuous dive for "no reason".

I suspect there are plenty of people who dive for a lifetime, never get a clinical bend but maybe grumble about "feeling old" and never get diagnosed with a PFO but had one the whole time.

 

[erikradstrom]

There are many instances of divers going for years without problem, then suffering DCS and having a large PFO discovered.

I can second that since I am one of them. I dived for many years before my first hit and after the first i got two more at shallow 30m dives with a month in between.
Never had anything before.
They found a 7mm PFO that I now closed but before closure I dived one year just with a change of GF.

It worked fine untill I did 3 days in a row, then I got bent again.

Every time I got skinbends on my left side, and then in some cases other symptoms as blurred vision (couldnt focus and saw stars), my arm got numb, pulmonary caugh and passing out.

It was like it accellerated after my first hit and I got it easier after that.

 

[Simon Mitchell]

Hello,

Mark's question about how one can have a PFO for years without problems is fascinating, and timely for me. The UHMS is running a workshop on PFO and DCS next week in Montreal, and I am giving a lecture on the pathophysiology of the PFO's role in the process. This is a question I will need to address.

Ben's answer is part of the story:

They are just lucky/statistically unfortunate due to flying inside the curve for much of the time- (trying desperately to steer the thread back on course ;-)
I have met the "I got bent, been diving the same way 20years and nothing then this!" type of disbelieving divers and on questioning you discover a perfect storm- cautious diving for 20years but now older, dehydrated from a few beers the night before, didn't sleep due to other snoring divers on trip, slight current, hard work with the DSMB reel and wham-bang= first bend on innocuous dive for "no reason".
I suspect there are plenty of people who dive for a lifetime, never get a clinical bend but maybe grumble about "feeling old" and never get diagnosed with a PFO but had one the whole time.

We think that the reason a diver can have a PFO for many years / dives and never have a problem is that for clinically obvious PFO-related DCS to occur a number of factors have to line up.

First (obviously) you have to have a PFO, and it probably has to be large because the very small ones don't allow much or any blood (and by implication venous gas emboli [VGE]) to cross from veins to arteries . Thus, about 30% of people have a PFO, but a much smaller proportion have a large PFO.

Second, you have to form VGE, and the critical point is that the more you form, the more likely a large number will be carried into the arteries if a small amount of blood crosses the PFO (see the next point). This is where Ben's points become relevant. How many VGE you form after a dive is probably highly variable and dependent on both your decompression profile and various other physiological factors some of which he mentions. We certainly don't form high grade VGE after every dive.

Third, blood has to cross the PFO when a large number of VGE are present in the right (venous) side of the heart. Some PFOs allow a small amount of blood to shunt spontaneously but most don't, and there needs to be some provocation (like lifting something heavy or straining for another reason) at the wrong moment. There have been many cases in which onset of symptoms was confluent with lifting or straining.

Fourth, the bubbles probably have to cross the PFO at a time when vulnerable tissues such as a the spinal cord, inner ear and skin remain supersaturated with inert gas after the dive. You might want to ask yourself why people don't get DCS when they have a strongly positive PFO test and lots of tiny bubbles go flying off into the arterial circulation in the cardiologists surgery. The answer almost certainly is that in a PFO test when the arterial circulation carries bubbles to the tissues, the tissues are not supersaturated with inert gas (which would cause the bubbles to grow). This is important because the time window in which the relevant tissues (especially inner ear and spinal cord) remain supersaturated after a dive is probably relatively short - probably 30 min to an hour. Thus, bubbles crossing a PFO after that would be much less likely to cause problems.

You can see that it is a bit like the swiss cheese model for an adverse event to occur. Most of these components of the model have been substantially or at the very least circumstantially proven. Thus, a diver can have a PFO, but a whole lot of things have to line up for it to be a problem. There may be other things we don't know about yet and Mark's theory about some contribution from cumulative damage can't be excluded.

Simon M

 

[Simon Mitchell]

Oh, and I meant to point this out earlier:

Once again we see you Simon taking every opportunity to make attacks against me... because I dare to stand up to his egotistical arrogance and fallacies.

It seems a bit disingenuous to whine about being "attacked" when you posted this....

Most in the science community recognize that fact, but a couple want to trick you into making a connection between tissue and venous micro-bubbles. Don't get sucked into the junk science fad.

....before I even came anywhere near this thread.

Simon M

 

[apitkin]

So this is really interesting. There are many observations which do not fit with a simplistic mechanism for PFOs causing DCS by permitting arterialization of VGE. These include:

1. People who have ASDs and PFOs diving aggressively for many years and not getting DCS
2. People who have their PFOs closed and still get DCS

I have had a nagging suspicion for a long time that the whole story is a lot more complex than we think. One possible hypothesis is that some people have an underlying vascular abnormality which may be responsible for both their DCS and their PFO (cardiac endothelium is similar to vascular endothelium, and the reason some people have a PFO is not well understood). This may explain why some divers continue to get DCS after their PFO is closed. Here is a paper from Germany looking at the association of endothelial dysfunction and PFO in patients with cryptogenic stroke.

Andy

 

[Ben Field]

2. People who have their PFOs closed and still get DCS

Well that's the same as saying "people without PFO's get DCS" which we know to be true.

More to the point is did someone get bent and that caused their PFO to be found, now its closed they still have the damage from the first bend making them more likely to get bent again.

As with almost anything Diving related there are not enough participants and data points to make many statistically viable statements from.

 

[cathal]

More to the point is did someone get bent and that caused their PFO to be found, now its closed they still have the damage from the first bend making them more likely to get bent again.
.

My understanding was that to date there was no evidence to support this theory i.e. once you get bent your more susceptible to get a bend than a diver who had never been bent.

Great discussion and thanks to to Simon for keeping it factual

Cathal

 

[Randy Thornton]

My understanding was that to date there was no evidence to support this theory i.e. once you get bent your more susceptible to get a bend than a diver who had never been bent.

Great discussion and thanks to to Simon for keeping it factual

Cathal

I am also curious about this. We hear divers, instructors, agencies, etc. imply that once bent a diver is more likely to be bent again. With the exception of a preexisting medical condition such as PFO or other vascular abnormality, is there really any evidence to suggest that "once bent, a diver is more likely to experience another bend?" Simon, Andy, or any of you other docs out there, any thoughts?

 

[GLOC]

A question more likely to get a better response would be, is a diver with a previous injury involving tissue damage more predisposed to DCS than before the injury?

DCS will cause tissue damage which may reduce blood flow to the region therefore leading to problems in off-gassing...

Regards

 

[Randy Thornton]

Gareth, I know that this is commonly taught in the industry/community, however I wonder if there is any actual data to support this theory.

A question more likely to get a better response would be, is a diver with a previous injury involving tissue damage more predisposed to DCS than before the injury?

DCS will cause tissue damage which may reduce blood flow to the region therefore leading to problems in off-gassing...

Regards

 

[Mark Chase]

Gareth, I know that this is commonly taught in the industry/community, however I wonder if there is any actual data to support this theory.

I massivly smashed my elbow when i was 13

Its now my early warning system for DCS

SO I beleive pre existing dammage resulting in DCS is a fact

ATB

Mark

 

[Simon Mitchell]

So this is really interesting. There are many observations which do not fit with a simplistic mechanism for PFOs causing DCS by permitting arterialization of VGE. These include:

1. People who have ASDs and PFOs diving aggressively for many years and not getting DCS
2. People who have their PFOs closed and still get DCS

I have had a nagging suspicion for a long time that the whole story is a lot more complex than we think. One possible hypothesis is that some people have an underlying vascular abnormality which may be responsible for both their DCS and their PFO (cardiac endothelium is similar to vascular endothelium, and the reason some people have a PFO is not well understood). This may explain why some divers continue to get DCS after their PFO is closed. Here is a paper from Germany looking at the association of endothelial dysfunction and PFO in patients with cryptogenic stroke.

Andy

Hi Andy,

Yes, as you can imagine, we have wrestled with these difficult issues for years. The strongest argument against PFO being a marker for some other contributory abnormality rather than being a simple venous to arterial conduit for bubbles is the undeniable and strong association between PFO size and DCS risk. Small PFOs that shunt a few bubbles even with provocation are not associated with any measurable increase in risk, but spontaneously shunting lesions have a strong association with cerebral, spinal, inner ear and cutaneous DCS. If PFO was simply a marker for some other biochemical or endothelial abnormality then this size-relationship with DCS risk would be unexpected (unless PFO size itself was also somehow an index of the biochem / endothelial abnormality which would seem a bit of a stretch).

The most plausible explanation for the "dive for years with a PFO but then have a problem" conundrum that we can come up with at this time is the "swiss cheese" model I described on the previous page (with the acknowledgement that there may be other unknown components). There are also several studies that have examined the possibility that PFOs can enlarge or at least change their shunting behaviour (jargon alert for non medics - that means their propensity to allow blood to cross from veins to arteries) as we get older (which could obviously contribute to increasing risk over time), but this is controversial and not a universal finding.

I am less troubled by the issue of people who have their lesion closed but still suffer DCS. For a start, the most common symptoms of DCS (musculoskeletal pain, patchy paraesthesias (jargon again - tingling), constitutional symptoms like fatigue) have never been linked to a PFO. Development of these symptoms does not seem to arise from VGE getting from veins to arteries. Thus, having a PFO fixed or not should not alter the risk. In addition, several of those forms of DCS that are associated with PFO such as spinal and inner ear DCS have other proven (non PFO-related) mechanisms such as bubble formation in the tissues themselves, and in the case of the spinal cord, bubble formation in the epidural veins which cause a venous infarction of the cord. Thus, it would be possible for a diver to suffer a PFO related spinal DCS, have the PFO fixed, and then suffer spinal DCS through another non-PFO related mechanism. Finally, because we increasingly understand that pulmonary shunts can occur in anyone, those 4 forms of DCS known to be associated with venous to arterial shunting of bubbles could occur through that mechanism in someone without a PFO (or with a fixed PFO). I always warn divers determined to have a PFO repair that their PFO may not have been the cause of their problem, and consequently, that the repair is not a cast iron guarantee that they won't suffer the same problem again.

Simon M

 

[GLOC]

Randy,

A quick search using "scar predisposition to decompression illness" in Google Scholar found these

Previous Injury . There are numerous accounts of bends pain occurring preferentially in areas that have been previously injured. No objective data are available for analysis to support this theory. However, injury may cause blood perfusion changes or deposition of scar tissue. It is possible that these changes decrease nitrogen washout rates and predispose bubble formation in these areas.

http://www.tanktigers.net/CHAP03R.PDF

http://archive.rubicon-foundation.o...dle/123456789/9781/DHM_V38N1_8.pdf?sequence=1 - but unfortunately SPUMS articles are badly encoded as PDFs so the search facility doesn't work

http://ww.ukdivers.net/misc/docs/DivingIllnesses.pdf

Alternatively, pulmonary barotrauma is an absolute contraindication to diving because the resultant lung scarring theoretically predisposes to further lung injury with pressure changes. I am not aware of any reports that have specifically investigated DCI incid- ence in divers with previous barotrauma.

http://www.ce4optometry.com/web/mediconcept/17.3White.pdf -

Scarring and alterations in local tissue may increase a divers risk.

From 1988 http://gtuem.praesentiert-ihnen.de/tools/literaturdb/project2/pdf/SPU01288.pdf -

3. There appears to be no association between CAGE in diving and:
(a) pre-existing scar tissue in lung or pleura8
(b) measured lung size10
(c) depth of the dive.