Your references state... "...decompression sickness..."
This diagram is of DCS injury. The animal was deliberately forced into a severe injury through aggressive procedure. We are looking at damage from a DCS injury. There is no fix or shallow stop to correct for that.
You are using a picture of severe injury, to then show it as evidence of normal VGE growth. Not good enough Simon - you know the difference. That is not normal VGE growth.
Ross, so now you are proposing that there is one mechanism of bubble formation for "normal VGE" (whatever those are), and one mechanism for bubbles that cause DCS (which you incorrectly portray as exclusively extravascular), even though it is a simple fact that all bubbles forming in a tissue, both intravascular and extravascular, must form from the same supersaturated inert gas. You are also implying that a deep stop approach to decompression can somehow allow there to be high numbers of VGE whilst magically protecting the diver from forming the real nasty bubbles that actually cause DCS. These notions are clearly implausible.
Conversely this example DCS injury presents you with a conundrum. If a neurological DCS injury, is partly the process of bursting of extravascular gas into the intravascular, then it stands to reason the higher VGE registered during neurologaic DCS events, comes from the injury site, and not normal VGE growth processes. Which would further enforce that high VGE in non-injured persons, is not a precursor to DCS (which is exactly the case now).
I have no idea what you are trying to say here.
Deco models are designed and calibrated to avoid DCS, so the extreme damage in the picture is unlikely to be part of normal diving, or VGE growth.
How do you know that is extreme damage? The tissue bubble rupturing into a capillary is one of the hypotheses to explain all VGE formation as I pointed out many pages ago. It is also hypothesised that bubbles might form on the surface of the cells that line tissue capillaries. Whatever the mechanism, it is unlikely it changes just because you are either within or in breach of your prescribed decompression limits.
You are then maneuvering to make VGE and tissue micro-bubbles the same thing, so you can pretend that bubble models don't work as more scare tactics.
No one is saying that VGE and tissue microbubbles are the same thing; VGE are in the venous blood, and tissue bubbles are in the tissue. What we
are saying is that you can't have high numbers of VGE leaving a tissue and claim that this is magically unrelated to the tendency for extravascular bubbles to be forming in the same tissue. They are all forming from the same supersaturated inert gas. If one is high, the other will tend to be high.
And once again, I remind you (as Neal has multiple times) that the elephant in the room in relation to your hand wringing about whether high VGE = high tissue bubbles is that high grade VGE are not harmless. So I don't need to "make VGE and tissue micro-bubbles the same thing" in order to raise concerns about the data showing bubble model decompressions result in more VGE. High VGE is sufficient concern of itself.
Then do some math to calculate the volume in that bubble, and see how much dissolved gas in saturated tissue is needed to make such a bubble, and ask yourself if it all comes from one capillary?
I think you have missed the point. You implied that a eg 50micron bubble could not come from a 5 micron capillary. Clearly it could.
So, none of the above is actually normal VGE, but instead serious DCS injury information.
Do you have any pictures of normal VGE growth?
The only place I have ever heard VGE called "normal" is in posts by you. What is "normal"? Low grade? Are you suggesting there is one mechanism of formation up to grade 1 or grade 2, but then above that the mechanism changes for some reason? And who really cares anyway...see "elephant in the room" above.
Do you have evidence that normal VGE is directly related to extravascular micro-bubbles
Leaving aside the inappropriate reference to VGE as "normal", given that we are only just developing the technology to accurately measure stationary bubbles it is clear that there are no correlations of VGE vs tissue bubbles. But it is difficult to see how the tendency of bubbles to form in the two locations can be unlinked given that within any tissue they both form from the same supersaturated inert gas.
The latest published Jay Buckey study describes the two bubble types as separate bubbles.
This is a gross misinterpretation of the study. The study was mainly about intravascular micro-bubbles (1 - 4 microns) and their relation with larger VGE. They only report tissue microbubbles in one site (a muscle) for one animal as far as I can see, and those tissue microbubbles behave in much the same way as the intravascular microbubbles in the same animal.
The Bennett Elliot makes it clear that extra/intra vascular bubble are different. Here is the introductory passage again:
"While pulmonary DCS can be explained entirely by the formation of inert gas bubbles in the venous blood (intravascular VGE), DCS in other organ systems described below may be due partly or entirely to bubble formation within the tissue themselves. [referring to: spinal, joint, fatty connective, inner ear]".
If you want to modify your view since writing that 10+ years ago, then do so, but please do not try to distort it into saying something else.
"Introductory passage??" I really hope a lot of readers have access to B&E so that they can gauge for themselves your misinterpretation of this work, or your dishonest wilful misrepresentation of it (it has to be one or the other). I wrote it Ross (except you added the "spinal, joint, fatty connective, inner ear"). I know what we said, and why we said it. The phrase you have cherry-picked is the first sentence in the chapter's
subsection entitled "
Inert gas bubbles in tissue"!!! We are hardly likely to open that section with a discussion of the importance of VGE are we? The phrase is entirely correct, and remains correct to this day. For example, we still think that musculoskeletal DCS is most likely caused by tissue bubbles. You could have picked many phrases from the section entitled "
Right to left shunting of venous bubbles" that would support the arguments I (and Neal) have been making about shunting of VGE and risk. One of those sentences is "There is evidence that such shunting is important in human disease (DCS)", followed by a description of the studies that were relevant at the time.
You ask about modified views. I can tell you that if the chapter were being written today, it would place more emphasis on "right to left shunting of venous bubbles" because a substantial number of important papers have emerged which demonstrate a higher incidence of large right to left shunt in divers with neurological DCS. These include:
Cantais et al. Right to left shunt and risk of decompression illness with cochleovestibular and cerebral symptoms in divers: case control study in 101 consecutive divers. Crit Care Med 2003;31:84-88.
Klingmann et al. Embolic inner ear decompression illness: correlation with right to left shunt. The Laryngoscope 2003;113:1356-61.
Torti et al. Risk of decompression illness among 230 divers in relation to the presence and size of patent foramen ovale. Eur Heart J 2004;25:1014-20.
Cartoni et al. Identification of professional scuba divers with patent foramen ovale at risk for decompression illness. Am J Cardiol 2004;94:270-3.
Gempp et al. Relation between right to left shunts and spinal cord decompression sickness in divers. Int J Sports Med 2009;30:150-3.
Ignatescu et al. Susceptibility of the inner ear structure to shunt-related decompression sickness. Aviat Space Environ Med 2012;83:1145-51.
Gempp et al. Inner ear decompression sickness in scuba divers. Eur Arch Otorhinolaryngol 2012;270:1831-7.
All of these papers imply that shunted VGE are important in the pathophysiology of various forms of neurological DCS, but you say,
in the face of overwhelming evidence to the contrary, that VGE don't matter and are separate to the bubbles that cause neurological manifestations.
Simon M
