Does the discussion on Helium Penalty affect the discussion/thought on ICD?

[packrat12]

I wanted to see from some of the experts what their thoughts were on Isobaric Counter Diffusion and how it relates with the information on the “Helium Penalty” that is currently being discussed. My question is that if we consider He/N2 as one gas, e.g. no Helium Penalty, do we then even consider ICD relevant? This question is related only to short scuba dives (<3hrs or so) and not to the medical field. I would think that the information should be the same no matter which side of the fence an expert is on but I am curious what the experts are thinking on it, i.e. is it Penalty = ICD, No Penalty = No ICD.

 

[Dr Simon Mitchell]

Hello, currently on a dive boat. Will reply to this tomorrow when we get back.

Simon M

 

[David Doolette]

Not really. The helium penalty information relates to the observation that helium and nitrogen half-times are probably similar in relatively fast exchanging tissues that control the early stops during decompression from most bounce dives. Although most gas exchange is primarily limited by the blood flow, there are a few places in the body where gas exchange is diffusion-limited and helium exchanges faster than and nitrogen. These will generally be very slow half-time tissues that control decompression from saturation dives or perhaps the shallower stops in very long bounce dive decompressions, say over ten hours. In these places a helium-to-nitrogen gas switch might accelerate the decompression. However, there are a couple places with unusual anatomy, the inner ear and the skin, where a helium-to-nitrogen switch can cause counterdiffusion problems. To describe the former as an example, inner ear has relatively large fluid-filled spaces which exchange gas only by diffusion with the surrounding tissue that has a blood supply and is the site of the sensory receptors. So the sensory tissue takes up gas from the blood, and then gas the diffuses into the fluid space, the reverse occurs with gas washout. During a heliox dive, these fluid spaces take up helium by diffusion, if that is followed by a helium-to-nitrogen switch, faster diffusion of helium from the fluid spaces into the sensory tissue than diffusion of nitrogen in the opposite direction can cause cause or enhance supersaturation in the sensory tissues. This seems only to manifest as a problem (inner ear DCS) after very deep dives.

David Doolette

 

[Dr Simon Mitchell]

David has answered the question.

Simon M

 

[The Chairman]

Very lucid replies that even a curmudgeon like me can understand. Thanks.

 

[David Doolette]

Just to follow up a bit more. The natural question is, “if helium is taken up faster than nitrogen into the inner ear fluid space faster, why doesn’t this impose a helium penalty, whereby the inner ear imposes a deeper first stop if diving heliox than trimix or nitrox?” This is a complicated issue, and indeed inner ear DCS does sometimes onset during decompression, characteristically not long after a helium-to-nitrogen switch, indicating either that the helium-to-nitrogen switch is implicated, or that the decompression up to that time (including obviously the deeper stops) was insufficient. I happen to believe the latter is the more important factor - so why no helium penalty? There are two issues to consider. First is because inner ear DCS during decompression typically occurs from dives deeper than 300 fsw (and unusually much deeper), which are conducted with mostly helium and probably inconsequential amounts of nitrogen, so there is no scope for a helium penalty to manifest – i.e. no one is conducting 400 fsw air dives to find out if they can get away with a bit shallower first stop than a comparable heliox dive.

Second, the inner ear might not be the “leading” tissue that imposes the first decompression stops. Much of my thinking about inner ear DCS is summarized in Mitchell and Doolette, Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving and Hyperbaric Medicine 2015;45:105-110. Here we summarize the data about inner ear DCS occurring following air and nitrox diving, where inner ear DCS is not uncommon and there is a lot of data. These data show that there is a strong associating with persistent (patent) foramen ovale (PFO) / right-to-left shunt of bubbles (RLS). More than 80% of the divers with inner ear DCS have RLS, compared to about 25% in the general population. This (and other circumstantial evidence) suggests that RLS of VGE through a PFO is the culprit in most inner ear DCS occurring after surfacing from these sort of dives. In that paper, we hypothesize that this same PFO mechanism might be the cause of inner ear DCS occurring during decompression from technical dives. So whereas supersaturation by decompression (with perhaps a small contribution from ICD) in the inner ear is important, you need to seed the inner ear with bubbles by RLS. There still is not enough data to confirm that hypothesis, but a paper published since showed that in five of eight (63%) technical divers who had inner ear DCS tested positive for PFO/RLS (Guenzani et al. Inner-ear decompression sickness in nine trimix recreational divers. Diving and Hyperbaric Medicine 2016;46:111-116.) If VGE are the culprit, then it may be that the tissues from which the VGE arise (that may not manifest any helium penalty), not the inner ear itself, that are the “leading” tissues during the relevant part of decompression.

It is noteworthy that inner ear DCS is usually associated with relatively aggressive decompression, whether it follows air / nitrox dives or occurs during decompression from deeper helium-based dives. When conducting deeper dives, my recommendation is to use conservative decompression and not assume that the levels of conservatism you use for say a 200 fsw dive are going to be adequate.

David Doolette

 

[RyanT]

Thank you for your response David. Here's a question though. Why aren't our joints as likely to suffer bubble formation resulting from ICD? Like the inner ear, the synovial fluid inside the joint capsule is somewhat isolated from the blood supply. I understand there are differences in tissue types, forming joint capsules versus the inner ear, but it seems like many of our joints would be prone to similar problems arising from ICD.

 

[David Doolette]

Ryan

There are a couple points to consider.

First, the anatomy is not identical and perhaps does not lend itself to development of sufficient supersaturation

Second, it may be that bubbles do form, and there is a single report of knee pain after a nitrox-to-heliox (the opposite of what we are concerned about) switch in a 100 fsw saturation dive. Bubbles may be less likely to cause a problem in a joint, whereas the inner ear is a more sensitive tissue. The sensory tissue or richly innervated with receptors that respond to the minute pressure waves and shear in the fluid from sound and rotation. It is easy to imagine them bring disturbed by a growing bubble.

 

[packrat12]

Thanks David and Simon for your inputs. I was curious where the thoughts may lead. Always a great and detailed response from both of you!

 

[RyanT]

Certainly their are differences in anatomical features between the inner ear connective tissues and joint capsules. Your point, however, about the sensitivity of the mechanorecptors in the ear, makes a lot of sense. Not sure why I didn't think of that, actually. Anatomy aside, it does make me wonder if ICD may influence synovial joints at higher rates than we know about, but simply go unnoticed relative to when it happens in the exquisitely sensitive inner ear. Thanks for your response, David!