Gas bubbles may not be the underlying cause of decompression illness

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Hello DDM,

Just to clarify this comment before "certain others" latch onto it. I presume you are not dismissing the importance of VGE that cross a right to left shunt in the pathophysiology of PFO-related DCS?

Simon

+1
Or even right to left intraparenchymal shunts in the face of large venous bubble loads even in the absence of a PFO. Hard to prove with transthoracic echo, but a likely hypothesis for the occasional case, in my mind.
 
Hello DDM,

Just to clarify this comment before "certain others" latch onto it. I presume you are not dismissing the importance of VGE that cross a right to left shunt in the pathophysiology of PFO-related DCS?

Simon

Hi Simon, of course not, thanks for asking. The way I read the paper, the authors were referring to detectable VGE, not necessarily shunted, which (for the benefit of "others") correlate poorly with DCS.

Best regards,
DDM
 
After ruminating a bit, I have to admit that I'm rather astonished that a reputable publisher like Elsevier publishes a journal like this. I

I'm waiting for Elsevier to come out with a new journal of "evolutionary biology hypotheses." I've got a ton of failed experiments, that I thought were great ideas, that could be published!
 
In all seriousness, I do appreciate the view of the authors that inflammation plays an important role in DCS. To suggest that bubbles really aren't important though is a bit laughable.
 
To deco experts. I need some help in understanding something. @Dr Simon Mitchell I would be interested in your views in particular.

This article: https://www.uhms.org/images/DCS-and-AGE-Journal-Watch/madden_gas_bubbles_med_hypot.pdf

Draws these conclusions:



My question is simple, although the answer may not be: What the heck are they talking about?

R..

This was published in 2008. Any peer review replies in this journal?

If this hypothesis is correct, shouldn't nitrox divers get dci symptoms more than air divers?

The article seems to ignore bubble formation and tissue damage that occurs outside of the blood vessels.

The hypothesis may help in furthering our understanding of the cascade of events that occur with dci, but I think the conclusion in the article is way, way off.
 
@Dr Simon Mitchell: " If oxygen exposure and oxidative stress (rather than inert gas bubbles) were the cause of decompression sickness, then we would expect it to be a common event among patients treated with hyperbaric oxygen.... but I don't believe there has been a single case of DCS, EVER, in millions of hyperbaric oxygen treatments."

My understanding is, they are not saying that oxidative stress alone is the cause of DCI; it "acts as a secondary insult" when bubbles are formed during decompression.
 
“Cold fusion” got published and was bogus. Paper of future novel price winners got rejected by some journals only to be published by other as groundbreaking discoveries. Science is not black and white but always corrects itself. Maybe the authors apply for grants and needed a paper to strengthen their case? In any case, if true we will see certainly see other in the field investigating this tangent.
You can't compare an exact science like physics with medicine. In physics, one can prove or disprove something with a single experiment. In medicine, proving or disproving something is way more complicated. Some people even claim medicine is an art, not a science. Everything medics say should be treated as their working hypothesis, not as an absolute truth. To give an example, we were always told that it is lactic acid that causes muscle pain after workouts. Until one day it was not lactic acid anymore. Stomach ulcer used to be caused by stress or too much coffee; now the main culprit is a bug called Helicobacter pylori. This uncertainty, however, makes way more room for hypothesizing in medicine than in physics.
 
My understanding is, they are not saying that oxidative stress alone is the cause of DCI; it "acts as a secondary insult" when bubbles are formed during decompression.

Hello,

I agree that there are quite a few mixed messages in the paper if you read the entire thing. It is not very well written.

Depending on which part you want to focus on / quote, you could form the impression you have, or the the opposite. For example, this section of the abstract seems quite declarative / explicit in suggesting bubble are secondary:

DCI is a potential problem for a growing population of professional and recreational divers. We hypothesise that these gas bubbles are not the causative agent in progression of DCI, rather an exacerbating factor. Endothelial dysfunction caused by a temporary loss of haemostasis due to increased total oxidant status is postulated to be the cause in this at-depth endothelial dysfunction hypothesis.

Perhaps the reason most of us in the game interpreted the paper to be suggesting bubbles are secondary to oxidative stress is that there is actually nothing much new in viewing the situation the other way around. We have always considered the endothelium to be a target for damage; primarily by bubbles but also by secondary inflammatory processes initiated by the bubbles and the damage they cause. Indeed, such mechanisms have been unequivocally proven in various high quality animal experiments.

Simon M
 
Well, I assume you are being snide and really understood what I was trying to say. Yes I mis-stated and took a shortcut expecting that anyone not being pedantic would undersatand what I was getting at..

I should have said if the computer algorithm allows you to monitor your dive and helps prevent DCI in most cases, if followed properly, does it really matter if it's bubbles or microparticles? Happy?

Yes. I too should shoulder some criticism of my post as you have been so decent in respect of yours, thank you.

It does matter if it is bubbles or micro particles because the algorithm is modelling gasses to control bubbles. You are right at the level that it is immaterial if the algorithm requires sufficient "off gassing" that the (now disputed) cause does not have an effect. Yes, I know that is what you meant and apologies for my over simplistic response.

Much arithmetic research has been done - much of it hypothetical - in order to perfect modern deco algorithms like the ZHL16 at the core of most commercial computers. But we all know and understand that human tissue does not come in 16 discrete groups with nitrogen half times of exact numbers of minutes. You can read many many discussions and debates on this and many other fora about abstract concepts like gradient factors. All these debates start from the assumption that we are managing gas dissolved in tissue and seeking the prevention of physical bubbles that block body functions in some way.

Any improvement in understanding of the physiology of how and why DCI occurs is a step forward. Confirmation that it is the physical characteristics of bubbles is equally valid as new data on any other possible causal factors. This paper offers up a hypothesis that has bearing on that. I doubt it (the paper) has much to offer but it is at least worth a read and some discussion (which is what has happened).

Discussion in the written format is much less effective than spoken conversation and sometimes can appear a bit antagonistic. However this has been and is a interesting and thanks to everyone who has contributed.
 

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