Doolette's Alert Diver Interview

[atdotde]

Any idea when this will make it into the repositories? Fedora in particular?

Also, it's been forever since I looked at any of the deep stops threads. Anyone have a quick guide to reading the heat maps?

It is unlikely that any future version of Subsurface will make it to the repositories since we decided this model does not work for end user applications (or at least for us): As I understand, Fedora currently ships version 4.4.2 which is now over 18 months old. A lot has happened since (for example VPM-B integration) and the distributions just don't catch up. In addition, Subsurface relies on very specific (and recent) versions of certain libraries which makes packaging non-trivial and ends up in frustrated users (and Subsurface getting complains about the program not running properly when actually the packaging is to blame).

The way out is the AppImage, a binary package that should work out of the box for any linux distribution (and yes, for some the current daily build has problems, we are working on that). This way of distributing software is very close to what is done on Windows and Mac and allows us to ship everything we need and make it just work. The program will inform you once there is a new version out and installing it is really not much more than a single mouse click. If you want to learn more about this decision, a good starting point is the Wikipedia article about Subsurface.

What the heat map shows you is the loadings of the tissues over time normalised to Bühlmann m-values (or gradient factors if you like). The main advantage is that you get an impression of the gas loadings (and thus supposed bubble feeding rate) of all tissues and not just the leading one. The main point in that thread was that the slow tissues are still on-gassing during the deeper stops (while they are not the leading tissue) and and that this way you get much more gas released than with shallower stops (which you cannot see if you only look at the leading tissue).

 

[Remy B.]

I saw the Videos from David Doolette and Simon Mitchell, and thank you it is better seen your explanation than getting the analogy description of Simon M, of a new guy like me discerning popo/kaka of the right information from Internet.

I hope both of you read this post and shine some light over this ignorant ( me ).

In my vast ignorance, I try to correlate different things like pro and cons, or what is good for one scenario lacks for other, I do this in order to create a balance.

for example, a Drag Car vs a Normal daily driver Car, both shine in their own scenario ( or for what they were build )

If you want the acceleration and torque/hp of a Drag car for sure you will not find it in a Normal daily driver car, and so you will not find in a drag car the comfortable and easy driving that you find in daily driver.

The balance came out to a Hot-road it is the merge of both to create the balance. ( kind of to say so )

In my introduction to Tec diving I was shown VPM, not understanding much of VPM nor GF, just that you want to keep bubbles small and low quantities, I followed the VPM and did my training with that, baby deco dives all good, no incidents and probably for VPM at those depths is no problem.

But because of my ignorance and reading the different topics and reports, I came to my own conclusion that I needed a balance both models had the pro and cons on fast and slow tissues.

So I opted for VPM +3 and padding my stops at 12-9 and 6m just add arbitrarily time to them.

After seen the Video from both of you, will I found what in my ignorance the balance is in GF-40/70 and probably will add time arbitrarily on 12-9 and 6m if I get to convince my buddies to do so.

But eventually there will be these dives where more experienced divers will follow X-model, and there will be always that controversy of my X-model never give me problems and others saying well but my X-model either and there will be me, trying to be conservationist, of course the best option is to not to do the dives, or to follow what I think is a balance, but then I will be kind of the black sheep of the group ( not too much of a concern, but it is always good to stay close to the group in the Deco Stops )

Simon, you where very neutral and stating, that you don't know actually where the deep stops shall start, you were certain about they were starting to deep, and after looking at your video I understand that yes we still on-gassing slow tissues in those deep stops, but it is that grey are of are we pushing to hard the fast tissues.

And my question is, ( maybe too simple as it is complicated ) will you guys David D and Simon M. conduct further research to find that balance, I guess the end goal is finding what give you the less type 1 and type 2 DCS incidents and not that one model give you less than Type 1 but more than Type 2 and vise-versa and is there are research about fast tissues problems in the Long term ?.

Same analogy to much of one good thing will end up hurting you because you took it too much, so pushing those fast tissues too much, can it cause problems that will show after years just to find out too late ?

I guess ( and maybe wrong ) a new Hybrid model needs to appear or more research on one model where the GF minimizes the impact in the Fast tissues, or vise-versa a VPM with stops that don't start that deep.

It will be kind of always the dilemma of Ford Vs Chevy and people in the confusion going for Dodge, at the end every one wants a Mercedes.

 

[Dr Simon Mitchell]

Simon, you where very neutral and stating, that you don't know actually where the deep stops shall start, you were certain about they were starting to deep.

Remy,

Your perceptive interpretation nicely sums up my position which is entirely based on the currently available evidence. I have stated many times that I don't know exactly where the deepest stops should start, but there are solid grounds for believing that bubble models probably start them too deep if you really do seek optimal decompression. The problem with further research is that the field is very poorly resourced for research. The only people who can easily do this sort of thing are groups like NEDU. I do hope more is done (there are a couple of related studies completed and in the publication pipeline), but it is very hard. I also cannot fault your "hybrid" approach, which is also a sensible application of the currently available evidence.

One cautionary note: I would be wary of trying to characterise different types of DCS as being related to fast or slow tissues. This is one aspect of the pathophysiology that some commentators on this subject have a poor grasp of. For example, tissues that are considered slow are probably responsible for producing most of the venous bubbles that appear after dives, and it is those venous bubbles that can cross a PFO, pass in the arterial blood to important tissues traditionally considered "faster", and cause problems there. In effect, this is slow tissue bubbles causing problems in faster tissues. Hope you can see what I mean.

Simon M

Simon M

 

[RyanT]

I guess the end goal is finding what give you the less type 1 and type 2 DCS incidents and not that one model give you less than Type 1 but more than Type 2 and vise-versa and is there are research about fast tissues problems in the Long term ?

Related to this statement, I have some concerns about the characterization of Type I verse Type II DCS. Clearly, there are cases where people have symptoms that they recognize as "pain only" and other cases where people have clear neurological symptoms. I had a discussion a number of years ago with a hyperbaric physician and he indicated to me that in virtually all "type I" cases he saw, he could also find evidence of neurological symptoms. In terms of short-term patient outcome, I'm sure that a Type I versus Type II diagnosis could be useful. I'm concerned though that in reality, DCS cases likely represent a continuum of tissue damage. Thus, I would suggest that we should be a little more careful with cases that we consider "basic type I" hits. I'd certainly be interested in hearing Simon M's thoughts on this.

 

[Remy B.]

Remy,

Your perceptive interpretation nicely sums up my position which is entirely based on the currently available evidence. I have stated many times that I don't know exactly where the deepest stops should start, but there are solid grounds for believing that bubble models probably start them too deep if you really do seek optimal decompression. The problem with further research is that the field is very poorly resourced for research. The only people who can easily do this sort of thing are groups like NEDU. I do hope more is done (there are a couple of related studies completed and in the publication pipeline), but it is very hard. I also cannot fault your "hybrid" approach, which is also a sensible application of the currently available evidence.

One cautionary note: I would be wary of trying to characterise different types of DCS as being related to fast or slow tissues. This is one aspect of the pathophysiology that some commentators on this subject have a poor grasp of. For example, tissues that are considered slow are probably responsible for producing most of the venous bubbles that appear after dives, and it is those venous bubbles that can cross a PFO, pass in the arterial blood to important tissues traditionally considered "faster", and cause problems there. In effect, this is slow tissue bubbles causing problems in faster tissues. Hope you can see what I mean.

Simon M

Simon M

Simon, thanks for you time and kind answer, I guess many of us are hoping more research is done, for the time I will follow the GF 40/70

 

[Dr Simon Mitchell]

Related to this statement, I have some concerns about the characterization of Type I verse Type II DCS. Clearly, there are cases where people have symptoms that they recognize as "pain only" and other cases where people have clear neurological symptoms. I had a discussion a number of years ago with a hyperbaric physician and he indicated to me that in virtually all "type I" cases he saw, he could also find evidence of neurological symptoms. In terms of short-term patient outcome, I'm sure that a Type I versus Type II diagnosis could be useful. I'm concerned though that in reality, DCS cases likely represent a continuum of tissue damage. Thus, I would suggest that we should be a little more careful with cases that we consider "basic type I" hits. I'd certainly be interested in hearing Simon M's thoughts on this.

Hello Ryan,

Thanks for your question. The Type I and Type II DCS terminology is confusing and not particularly useful because classifying DCS in this way is not reliably prognostic. For example, the most common "neurological" symptom (therefore technically Type II) is patchy paraesthesias (tingling) in the skin, but expert consensus agrees that this symptom is "mild" and self limiting, even in the absence of recompression.

In 2004 the UHMS ran a workshop which defined "mild DCS" which was the original intent of the so-called "Type I" classification. The symptoms considered "mild" were musculoskeletal pain, skin rash, fatigue, and patchy tingling (without objective numbness). The purpose of defining a DCS syndrome that could be considered "mild" was to identify cases in which long term harm was unlikely to accrue from not recompressing the patient. For example, if a diver at Bikini Atoll developed symptoms that met the mild designation, it would be a reasonable decision not to spend $50,000 evacuating them, but rather treat locally with surface oxygen and other adjuncts. That was not to say that you would not recompress such cases if recompression were easily available.

There is a BIG caveat on this however, and it recognises the same point that your diving physician acquaintance made to you. The UHMS workshop agreed that the mild designation could not be applied in the absence of a competent neurological examination (that is, a neurological examination by someone properly trained and experienced which essentially means a doctor). This stipulation recognised the advice you received that sometimes there are neurological manifestations that are unrecognised by the patient themselves. I think your dive doctor was over-calling it in saying "virtually all" Type I cases had neurological manifestations. I have examined many cases that are apparently mild and found no neurological signs. The findings of the workshop have been invoked for many divers with mild DCS in remote locations (after proper examination) and there is no signal in case reports or discussion amongst colleagues that the workshop decisions were unwise. Nevertheless, your point is well made; some seemingly "mild" cases do have neurological problems that a good examination can detect.

Reference: MITCHELL SJ, DOOLETTE DJ, WACHOLZ 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

Simon M

 

[RyanT]

@Simon M, thanks, that was enlightening! If I recall correctly, what the physician was telling me was that he performed a set of simple, cognitive skills tests, pre and post recompression treatment. These tests consisted of simple memory/logic tests requiring information assembly or recall over time spans lasting less than a minute, often 30 seconds. I suspect any cognitive deficit on that scale is not something most people would notice without explicit testing. At any rate, the physician said in all cases of Type I hits, he saw improvement in patients in the post treatment tests. As a result he said he no longer believed in "pain only" bends.

 

[Michael Guerrero]

So a Type I hit will also mean you're probably slightly buzzed (for the drinkers in the crowd) due to the bubbles surging through your body and likely hitting the arterial side and the tissues nearby. Seems to make sense.

 

[Kevrumbo]

There's a continuum of symptom severity within the type I DCS designation as well, from "sub-clinical" fatigue, to tingling and the "niggles" (short dull stabs of musculoskeletal achiness), to frank, acute impulses of intractable limb/joint pain. Obviously a patient suffering the latter would not characterize the injury as "mild", and would insist on immediate recompression. . .

 

[Dr Simon Mitchell]

@Simon M, thanks, that was enlightening! If I recall correctly, what the physician was telling me was that he performed a set of simple, cognitive skills tests, pre and post recompression treatment.............the physician said in all cases of Type I hits, he saw improvement in patients in the post treatment tests. As a result he said he no longer believed in "pain only" bends.

Hello again Ryan,

I don't doubt your physician is correct about some cases but his or her view of applicability to virtually all mild cases is not widely shared in the diving medicine community. The sort of cognitive skills evaluations mentioned are notoriously difficult to perform correctly / meaningfully and it would be easy to form an erroneous view on the matter. For example, in simple cognitive function testing there is a significant practice effect across the first couple of test repetitions. So two tests performed either side of a hyperbaric treatment might seem to indicate improvement whether the subject initially had real impairment or not. Similarly, there is a substantial expectation of benefit associated with recompression treatment so it would not be surprising if someone performed better in cognitive function testing after such a treatment even if there was no initial organic injury, just because they were subconsciously trying harder or expecting to be better.

Simon M