Cutting Edge Bubble study indicates possible damage to circulatory system

[npollock]

Hi Neal,

Could you clarify this? Do you mean that bubbles will deform (and may therefore squeeze through), or that bubbles will squeeze through (by changing shape), and therefore cannot form plugs?

It is known in microfluidic applications that gas bubbles can form plugs. See for instance http://www.me.iastate.edu/files/2011/09/nanotech_final.pdf . Especially in the presence of parallel channels taking up the pressure. Obviously this is not biology, so one needs to be careful, but still...

Cheers,

Matthieu

I chose "may" with intention. While bubbles moving in response to fluid pressure will distort to fit through small openings, there can also be situations in which effective stasis may develop. If flow stagnates, bubbles could sit rather than be pushed sufficiently to distort and move. In some cases, stasis could contribute to an effective "plug." Fluid pressures and effects are related.

It is important to be careful with definitive statements. The physiological state is dynamic.

Neal Pollock

 

[emmbee]

Fair enough. It reads 'will' at the moment, hence my confusion.

Thanks very much.

Matthieu

 

[Simon Mitchell]

I would think that DAN with its mountain of data and access, could come up with some meaningful trend lines for treatment numbers, and overall total tech diver number trends. But lets be honest - a declining treatment rate doesn't fit the narrative, doesn't help the insurance sales business, .

Another conspiracy theory. First you suggest that 3 diving medicine societies have conspired to provide advice that will result in harm to more divers in order to boost hyperbaric treatment numbers, and now you are suggesting that DAN is concealing data that show a trend towards increased safety in technical diving in order to preserve insurance sales. Ross, mostly the correct explanation for things is simplest one. In the case of the diving medicine societies they provide the advice on PFO that they consider to be most appropriate, and in DANs case they release data they actually have.

and goes against one influential person agenda

Oh really? That "influential person" is one of the few who has actually PUBLISHED data showing a decline in treatment NUMBERS (as distinct from rates) in all comers (not tech diving specifically). So how do you justify an inference that there is an opposite agenda?

HAAS RM, HANNAM JA, SAMES C, SCHMIDT R, TYSON A, FRANCOMBE M, RICHARDSON D, MITCHELL SJ. Decompression illness in divers treated in Auckland, New Zealand 1996-2013. Diving Hyperbaric Med, 44, 20-25, 2014

What you will note, however, is that the decline in treatment numbers was paralleled by a similar decline in new diver certifications over the same period. In other words, the decline in treatments could be explained by a decline in participation.

From the public information we have DAN + BSAC reports, at least 4 studies, various bits, and simple deductions, over the last 15 years we can say that tech treatment rates have been in a slow decline, while tech diver participation has grown significantly.

Neal has already told you (in his first post) that "we do not have good injury rate estimates". Anyway, no, we can't say either of the things you suggest, particularly the one about tech treatment rates. Unless you have an accurate numerator (new DCS cases - specifically of tech divers in this case) and a denominator (an index of diving activity specifically by tech divers) both recorded over time, then your claim is completely invalid.

In addition, as Neal has said, DCS is under-reported so any numerator estimate is almost certainly NOT accurate. You, of course, have accused me of fabricating such claims in the past. Do you think Neal is fabricating this too?

If you truly believe you have access to data showing tech treatment RATES changing over time, then put it on here. Let's see it.

During the same period the predominant deco was deeper stops, VPM-B, or GF emulations of that style. Obviously we were all heading in the right direction, by design or by luck.

I trust you will have noted that Dr Pollock's explanation for any recent increase in decompression safety among tech divers is essentially the opposite to yours.

Finally please tell us your thoughts on how arterialized VGE do not block the capillary, but instead elongate and pass through the capillaries (elaborate on the recent BSAC question period answer you gave). I think many here will find that an interesting point of view.

I suspect what Ross is trying to insinuate is that because these bubbles redistribute they don't matter. I will return to this later. I have to go to the OR now.

Simon

 

[emmbee]

During the same period the predominant deco was deeper stops, VPM-B, or GF emulations of that style. Obviously we were all heading in the right direction, by design or by luck.

I trust you will have noted that Dr Pollock's explanation for any recent increase in decompression safety among tech divers is essentially the opposite to yours.

I would like to add, since the subject has come up in this thread, that THIS is a case of "correlation is not causation".
There is a correlation (well apparently it's questionable to say the least, but for the sake of the argument let's assume that there is) between reduced rates of DCS and adoption of deep stops. This is when the wise person remembers "correlation is not causation" before jumping to the conclusion. "Obviously" is completely out of place.

Finally please tell us your thoughts on how arterialized VGE do not block the capillary, but instead elongate and pass through the capillaries (elaborate on the recent BSAC question period answer you gave). I think many here will find that an interesting point of view.

I suspect what Ross is trying to insinuate is that because these bubbles redistribute they don't matter.

To be honest, that's why I wanted to be clear on what Neal Pollock's thoughts on the matter were.

And I note that while the papers highlighting the discrepancies in the proportions of divers with a PFO between those who have had some type of bend and those who have not invariably triggers endless discussions about "why those people should not be allowed to dive", a reasonable explanation (other than bubbles, that is) as to why the discrepancy exists in the first place is still not forthcoming.

Cheers,

Matthieu

 

[Simon Mitchell]

Finally please tell us your thoughts on how arterialized VGE do not block the capillary, but instead elongate and pass through the capillaries (elaborate on the recent BSAC question period answer you gave). I think many here will find that an interesting point of view.

Ross, your quest to find some flaw in my pathophysiological arguments about VGE (in this case arterialized VGE) is not going to bear fruit because I am simply telling the truth about our current understanding of DCS. You are trying to rewrite pathophysiology in an attempt to deflect criticism of decompression profiles that produce a lot of VGE. It won't work because the currently available evidence does not support your views.

Anyway, the passage of bubble through capillary beds is not a "point of view". Like most things scientists like Neal and I would say in a presentation (or on a forum like this) it is a proven fact. This, however, does not render the impact of bubbles in a tissue capillary bed a benign event (as I suspect you are hoping) for reasons I will get to below. Neal can write his own reply if he wishes, but he has heard me deliver what I about to say to his diving medicine courses for doctors at least 6 times, and I am confident he does not disagree with any of it.

An arterial bubble entering a tissue capillary bed can have 3 fates depending primarily on its size, the arterial blood pressures, and the tissue supersaturation state.

A large bubble (bigger than typical VGE) may block blood vessels if it is long enough to occupy 3 generations of branching arterioles. In this setting the surface tension forces at the hemispherical gas-liquid interface at the leading ends of the bubble typically generate a force opposing progress that is greater than the surface tension force generated at the trailing end coupled with arterial pressure (which together promote progress). This paradigm was established in Des Gorman's PhD work (his thesis was entitled "The redistribution of arterial gas emboli").

Smaller bubbles can redistribute through the microcirculation (that is, pass right through the capillaries without lodging), and this is the most likely fate for small bubbles such as VGE. It seems some degree of this can be tolerated even in the brain, but it cannot be characterised as a benign event. It has been demonstrated that bubbles passing through a blood vessel damage the endothelial lining of the blood vessel inciting the migration of white blood cells to the site of damage, and a secondary inflammatory injury caused by activation of those white cells. The bubbles in some of these experiments were larger than VGE (though still small enough to redistribute), but VGE are big enough to be in constant contact with the endothelial wall when passing through a capillary, and will inevitably slide along it like a larger (longer) bubble. As such there is little reason to believe that they will not incite the same inflammatory processes. Anyone interested in reading about this could look at:

Helps SC, Parsons DW, Reilly PL, Gorman DF. The effect of gas emboli on rabbit cerebral blood flow. Stroke. 1990;21:94–9.

Helps SC, Meyer-Witting M, Reilly PL, Gorman DF. Increasing doses of intracarotid air and cerebral blood flow in rabbits. Stroke. 1990;21:1340–5.

Dutka AJ, Kochanek PM, Hallenbeck JM. Influence of granulocytopenia on canine cerebral ischaemia induced by air embolism. Stroke. 1989;20:390–5.

Helps SC, Gorman DF. Air embolism of the brain in rabbits pretreated with mechlorethamine. Stroke. 1991;22:351–4.

Collectively these studies demonstrated the inflammatory damage that arterial bubbles are capable of producing in the brain even when they are small to pass through the capillary beds, and also that this damage could be virtually eliminated by removing the white blood cells from the animals.

The third fate that may befall a small bubble (VGE size) is likely if it enters the capillary bed of a tissue that remains supersaturated with inert gas early after a dive. In this setting the bubble is likely to grow as dissolved supersaturated gas diffuses into the bubble. This mechanism has been proposed as the explanation for the association between inner ear, spinal and skin DCS and PFO because all of these tissue are likely to remain supersaturated for a period that corresponds to the appearance of VGE after diving. If the diver were to develop a large VGE load, and then shunted some VGE across a PFO (eg lifting or straining at the wrong time) and those VGE found their way to the supersaturated tissue, then the extra bubble growth could cause problems that might not otherwise occur. Anyone interested in this could look at:

Wilmshurst P, Bryson P. Relationship between the clinical features of decompression illness and its causes. Clin Sci (London). 2000;99:65-75.

Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: The role of tissue gas supersaturation. J Appl Physiol. 2009;106: 298–301.

Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperbaric Med 2015;45:105-110.

In summary, yes, small bubbles may redistribute through capillary beds, but there is considerable reason to believe that this is not benign. In addition, if VGE enter the tissue circulation of an organ that remains supersaturated at the time, the resulting growth in these tiny bubbles may cause a problem that would not otherwise have occurred.

Simon M

 

[rossh]

I ask Neal to share some information that I know others will appreciate. You then twist that request to imply something I never said, or suggested. You also made up a lot of fictitious and stupid accusations further up the thread.

You made a nice informative answer above, but you prefaced it with a bunch of rubbish, a straw man argument you invented with implied phony accusations about me.

We can all see you are straight back to your malicious and vindictive ways.... It seems the real Simon Mitchell is a mean and miserable a.......

.

 

[Simon Mitchell]

I ask Neal to share some information that I know others will appreciate. You then twist that request to imply something I never said, or suggested. You also made up a lot of fictitious and stupid accusations further up the thread.

Ross, you have spent years and countless posts arguing that VGE are normal and essentially harmless. You will have to forgive me for thinking that your question about how they don't block blood vessels was somehow related to that particular interest of yours.

Simon M

 

[emmbee]

An arterial bubble entering a tissue capillary bed can have 3 fates depending primarily on its size, the arterial blood pressures, and the tissue supersaturation state.

A large bubble (bigger than typical VGE) may block blood vessels if it is long enough to occupy 3 generations of branching arterioles. In this setting the surface tension forces at the hemispherical gas-liquid interface at the leading ends of the bubble typically generate a force opposing progress that is greater than the surface tension force generated at the trailing end coupled with arterial pressure (which together promote progress). This paradigm was established in Des Gorman's PhD work (his thesis was entitled "The redistribution of arterial gas emboli").

Smaller bubbles can redistribute through the microcirculation (that is, pass right through the capillaries without lodging), and this is the most likely fate for small bubbles such as VGE. It seems some degree of this can be tolerated even in the brain, but it cannot be characterised as a benign event. It has been demonstrated that bubbles passing through a blood vessel damage the endothelial lining of the blood vessel inciting the migration of white blood cells to the site of damage, and a secondary inflammatory injury caused by activation of those white cells. The bubbles in some of these experiments were larger than VGE (though still small enough to redistribute), but VGE are big enough to be in constant contact with the endothelial wall when passing through a capillary, and will inevitably slide along it like a larger (longer) bubble. As such there is little reason to believe that they will not incite the same inflammatory processes. Anyone interested in reading about this could look at:

Helps SC, Parsons DW, Reilly PL, Gorman DF. The effect of gas emboli on rabbit cerebral blood flow. Stroke. 1990;21:94–9.

Helps SC, Meyer-Witting M, Reilly PL, Gorman DF. Increasing doses of intracarotid air and cerebral blood flow in rabbits. Stroke. 1990;21:1340–5.

Dutka AJ, Kochanek PM, Hallenbeck JM. Influence of granulocytopenia on canine cerebral ischaemia induced by air embolism. Stroke. 1989;20:390–5.

Helps SC, Gorman DF. Air embolism of the brain in rabbits pretreated with mechlorethamine. Stroke. 1991;22:351–4.

Collectively these studies demonstrated the inflammatory damage that arterial bubbles are capable of producing in the brain even when they are small to pass through the capillary beds, and also that this damage could be virtually eliminated by removing the white blood cells from the animals.

The third fate that may befall a small bubble (VGE size) is likely if it enters the capillary bed of a tissue that remains supersaturated with inert gas early after a dive. In this setting the bubble is likely to grow as dissolved supersaturated gas diffuses into the bubble. This mechanism has been proposed as the explanation for the association between inner ear, spinal and skin DCS and PFO because all of these tissue are likely to remain supersaturated for a period that corresponds to the appearance of VGE after diving. If the diver were to develop a large VGE load, and then shunted some VGE across a PFO (eg lifting or straining at the wrong time) and those VGE found their way to the supersaturated tissue, then the extra bubble growth could cause problems that might not otherwise occur. Anyone interested in this could look at:

Wilmshurst P, Bryson P. Relationship between the clinical features of decompression illness and its causes. Clin Sci (London). 2000;99:65-75.

Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: The role of tissue gas supersaturation. J Appl Physiol. 2009;106: 298–301.

Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperbaric Med 2015;45:105-110.

Very interesting.

Thanks very much.

Matthieu

 

[silent running]

I ask Neal to share some information that I know others will appreciate. You then twist that request to imply something I never said, or suggested. You also made up a lot of fictitious and stupid accusations further up the thread.

You made a nice informative answer above, but you prefaced it with a bunch of rubbish, a straw man argument you invented with implied phony accusations about me.

We can all see you are straight back to your malicious and vindictive ways.... It seems the real Simon Mitchell is a mean and miserable a.......

.

Hi Ross, it's been a while, but apparently not long enough, as you still have not learned to argue whatever point you think you have without lowering the level of discourse, nor show any concern for how you come accross. Your bad faith and lack of humility are intolerable, and more people ought to tell you so. At this point on yet another site, it's now embarrassing in a global sense.

If you had a point of reasonable doubt, presented it politely and agreed to disagree with whomever you came up against, even if it were often, people would respect your intentions at least. As opposed to spewing vitriol such that your intentions seem much less than clear and much less than respectable...

 

[David Doolette]

Since this thread has involved some discussion about fitness to dive with a PFO, I would like to comment.

Let me start first by saying there is strong circumstantial evidence that right-to-left shunt (RLS) of venous gas emboli (VGE) through a PFO can cause some manifestations of DCS (in particular rapid onset CNS manifestations, notably inner ear DCS), most of this evidence has been cited in this thread. There is the higher prevalence of PFO in divers with these forms of DCS than in divers without these forms of DCS.(1,2) The RLS of VGE through a PFO is a plausible pathophysiological mechanism. (1) There is a reduced incidence of DCS in divers with PFO after adopting diving practices aimed at reducing VGE.(3) There is a reduced incidence of DCS in divers with PFO after PFO closure (4).

I want to comment the idea of pre-screening technical diver candidates for presence of PFO (i.e. screening divers who have never had an episode of DCS) so that divers with a PFO might have a prophylactic PFO closure. I do not think this notion has much traction, but still want to speak to anyone who might consider this as a policy or personal decision. I believe is not a good idea (even if you could find a cardiologist who would perform a prophylactic closure for diving).

There has been some comments about the cost / benefit of pre-screening, and that is certainly a factor. One rough estimate is that 1000 divers would need to be screened and 50 PFOs closed to prevent one case of DCS. (2) This is important for a policy decision but it has been noted that that might not matter to the individual diver. However, any individual considering pre-screening should consider some risks. First is the incidence of DCS in divers with PFO. Our best evidence (which is not strong but is improving) suggests that the incidence of DCS is about 2/10,000 dives without a PFO and about 5/10,000 dives with a PFO.(5) Compare this to the incidence of complications from PFO closure (death, cerebrovascular events, pericardial effusion, arrhythmias, and device thrombosis, malposition, erosion, and fracture) which is about 600/10,000 closures.(6) Obviously you need to put these numbers in the context that a diver will only have one closure and perform many dives, but it is far from certain a prophylactic closure makes any sense.

David Doolette

1. Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperb Med 2015;45:105-10.

2. Bennett,M.H. Evidence synthesis from the Australian experience. In Denoble,P.J. and Holm,J.R. Patent foramen ovale and fitness to dive consensus workshop proceedings. 2015 June 17; Montreal. Durham (NC): Divers Alert Network; 2015

3. Klingmann C. Lower risk of decompression sickness after recommendation of conservative decompression practice in divers with and without vascular right-to-left shunt. Diving Hyperb Med 2012;42:146-50.

4. Billinger M, Zbinden R, Mordasini R, Windecker S, Schwerzmann M, Meier B et al. Patent foramen ovale closure in recreational divers: effect on decompression illness and ischaemic brain lesions during long-term follow-up. Heart 2011;97:1932-7.

5. Germonpre,P. Incidence of DCS in divers with RLS – a prospective study. In Denoble,P.J. and Holm,J.R. Patent foramen ovale and fitness to dive consensus workshop proceedings. 2015 June 17; Montreal. Durham (NC): Divers Alert Network; 2015

6. Abaci,A. et al. Short and long term complications of device closure of atrial septal defects and patent foramen ovale: met-analysis of 28,142 ptients from 203 studies. Cath Cardiovasc Interv 2013;82:1123-1138.

 

[silent running]

Since this thread has involved some discussion about fitness to dive with a PFO, I would like to comment.

Let me start first by saying there is strong circumstantial evidence that right-to-left shunt (RLS) of venous gas emboli (VGE) through a PFO can cause some manifestations of DCS (in particular rapid onset CNS manifestations, notably inner ear DCS), most of this evidence has been cited in this thread. There is the higher prevalence of PFO in divers with these forms of DCS than in divers without these forms of DCS.(1,2) The RLS of VGE through a PFO is a plausible pathophysiological mechanism. (1) There is a reduced incidence of DCS in divers with PFO after adopting diving practices aimed at reducing VGE.(3) There is a reduced incidence of DCS in divers with PFO after PFO closure (4).

I want to comment the idea of pre-screening technical diver candidates for presence of PFO (i.e. screening divers who have never had an episode of DCS) so that divers with a PFO might have a prophylactic PFO closure. I do not think this notion has much traction, but still want to speak to anyone who might consider this as a policy or personal decision. I believe is not a good idea (even if you could find a cardiologist who would perform a prophylactic closure for diving).

There has been some comments about the cost / benefit of pre-screening, and that is certainly a factor. One rough estimate is that 1000 divers would need to be screened and 50 PFOs closed to prevent one case of DCS. (2) This is important for a policy decision but it has been noted that that might not matter to the individual diver. However, any individual considering pre-screening should consider some risks. First is the incidence of DCS in divers with PFO. Our best evidence (which is not strong but is improving) suggests that the incidence of DCS is about 2/10,000 dives without a PFO and about 5/10,000 dives with a PFO.(5) Compare this to the incidence of complications from PFO closure (death, cerebrovascular events, pericardial effusion, arrhythmias, and device thrombosis, malposition, erosion, and fracture) which is about 600/10,000 closures.(6) Obviously you need to put these numbers in the context that a diver will only have one closure and perform many dives, but it is far from certain a prophylactic closure makes any sense.

David Doolette

1. Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperb Med 2015;45:105-10.

2. Bennett,M.H. Evidence synthesis from the Australian experience. In Denoble,P.J. and Holm,J.R. Patent foramen ovale and fitness to dive consensus workshop proceedings. 2015 June 17; Montreal. Durham (NC): Divers Alert Network; 2015

3. Klingmann C. Lower risk of decompression sickness after recommendation of conservative decompression practice in divers with and without vascular right-to-left shunt. Diving Hyperb Med 2012;42:146-50.

4. Billinger M, Zbinden R, Mordasini R, Windecker S, Schwerzmann M, Meier B et al. Patent foramen ovale closure in recreational divers: effect on decompression illness and ischaemic brain lesions during long-term follow-up. Heart 2011;97:1932-7.

5. Germonpre,P. Incidence of DCS in divers with RLS – a prospective study. In Denoble,P.J. and Holm,J.R. Patent foramen ovale and fitness to dive consensus workshop proceedings. 2015 June 17; Montreal. Durham (NC): Divers Alert Network; 2015

6. Abaci,A. et al. Short and long term complications of device closure of atrial septal defects and patent foramen ovale: met-analysis of 28,142 ptients from 203 studies. Cath Cardiovasc Interv 2013;82:1123-1138.

Hi David, thank you very much for all your contributions to the discussion. I understand that a prophylactic closure of a PFO presents real risks, but wouldn't being screened for it and knowing whether or not you have one be at least of value for determining one's deco practices regarding things like physical regimen and computer conservatism?

 

[rossh]

Since this thread has involved some discussion about fitness to dive with a PFO, I would like to comment.

Let me start first by saying there is strong circumstantial evidence that right-to-left shunt (RLS) of venous gas emboli (VGE) through a PFO can cause some manifestations of DCS (in particular rapid onset CNS manifestations, notably inner ear DCS), most of this evidence has been cited in this thread. There is the higher prevalence of PFO in divers with these forms of DCS than in divers without these forms of DCS.(1,2) The RLS of VGE through a PFO is a plausible pathophysiological mechanism. (1) There is a reduced incidence of DCS in divers with PFO after adopting diving practices aimed at reducing VGE.(3) There is a reduced incidence of DCS in divers with PFO after PFO closure (4).

I want to comment the idea of pre-screening technical diver candidates for presence of PFO (i.e. screening divers who have never had an episode of DCS) so that divers with a PFO might have a prophylactic PFO closure. I do not think this notion has much traction, but still want to speak to anyone who might consider this as a policy or personal decision. I believe is not a good idea (even if you could find a cardiologist who would perform a prophylactic closure for diving).

There has been some comments about the cost / benefit of pre-screening, and that is certainly a factor. One rough estimate is that 1000 divers would need to be screened and 50 PFOs closed to prevent one case of DCS. (2) This is important for a policy decision but it has been noted that that might not matter to the individual diver. However, any individual considering pre-screening should consider some risks. First is the incidence of DCS in divers with PFO. Our best evidence (which is not strong but is improving) suggests that the incidence of DCS is about 2/10,000 dives without a PFO and about 5/10,000 dives with a PFO.(5) Compare this to the incidence of complications from PFO closure (death, cerebrovascular events, pericardial effusion, arrhythmias, and device thrombosis, malposition, erosion, and fracture) which is about 600/10,000 closures.(6) Obviously you need to put these numbers in the context that a diver will only have one closure and perform many dives, but it is far from certain a prophylactic closure makes any sense.

David Doolette

1. Mitchell SJ, Doolette DJ. Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale. Diving Hyperb Med 2015;45:105-10.

2. Bennett,M.H. Evidence synthesis from the Australian experience. In Denoble,P.J. and Holm,J.R. Patent foramen ovale and fitness to dive consensus workshop proceedings. 2015 June 17; Montreal. Durham (NC): Divers Alert Network; 2015

3. Klingmann C. Lower risk of decompression sickness after recommendation of conservative decompression practice in divers with and without vascular right-to-left shunt. Diving Hyperb Med 2012;42:146-50.

4. Billinger M, Zbinden R, Mordasini R, Windecker S, Schwerzmann M, Meier B et al. Patent foramen ovale closure in recreational divers: effect on decompression illness and ischaemic brain lesions during long-term follow-up. Heart 2011;97:1932-7.

5. Germonpre,P. Incidence of DCS in divers with RLS – a prospective study. In Denoble,P.J. and Holm,J.R. Patent foramen ovale and fitness to dive consensus workshop proceedings. 2015 June 17; Montreal. Durham (NC): Divers Alert Network; 2015

6. Abaci,A. et al. Short and long term complications of device closure of atrial septal defects and patent foramen ovale: met-analysis of 28,142 ptients from 203 studies. Cath Cardiovasc Interv 2013;82:1123-1138.

Hello David,


On the subject of PFO screening:

You argument David (like others), about forced PFO testings and mandatory operations, is not relevant to the real world choices.

No one is forced to go diving. No one is forced to have an operation. Diving is not a human right, and deco diving is not something everyone must be allowed to do, regardless of their physical state.

One rough estimate is that 1000 divers would need to be screened and 50 PFOs closed to prevent one case of DCS.

That won't happen. The real option is 50 new divers get to make a choice, before they ever start tech diving. Choices: a/ cancel all thoughts of becoming a tech diver, b/ get tested and possibly get the operation, c/ ignore it and apply extra safe techniques and hope it works.

Existing divers who request a screening, make a choice: a/ stop being a tech diver, b/ get tested and possibly get the operation, c/ ignore it and apply extra safe techniques and hope it works.


If screening (not testing) was recommended for all new people contemplating higher risk diving (work, mil, tech), then these new people would discover the issue BEFORE they start the high risk diving. IF they really want to still go tech diving, then they have to face up to their personal disadvantages, and consequences.

All that's needed is a recommendation - new tech / work divers should be screened for the condition, made aware of their elevated risk, and their increased likelihood of them getting injured.


That simple screening step would cut our future treatment rates in half, and eliminate countless more smaller injuries that go untreated.




*************************


Referring to your paper: Mitchell SJ, Doolette DJ. Selective vulnerability of the inner ear to decompression sickness in divers with right to left shunt: The role of tissue gas supersaturation. J Appl Physiol. 2009;106: 298–301.


It makes the case for the interaction of inner ear supersaturation, and occasional arterialized VGE, and implies blocking and causing localized off gas changes during the initial surface period. In the figure 1, and throughout the paper, it uses the sample dive of a 100ft on air for 25 mins, with a direct (NDL) ascent. The emphasis is put on the 8.8min half time of the inner ear, being supersaturated for the same period that surface VGE is typically reaching its peak. i.e. an overlapping period.


However, these same conditions do not exist in decompression diving. A simple deco dive with 30+ mins of deco, no longer has supersaturation in the inner ear (8.8 min half time) upon surfacing. The inner ear has off gassed enough in the deco stops, and typically falls below the supersaturation condition during the 20 ft stop.

The inner ear supersaturation condition upon surfacing and during the last stops, is further reduced and eliminated through higher fO2 deco mix, and the overlapping condition is effectively removed on O2 deco or with CCR use.

Further more, extended use of oxygen deco mix on longer deco, causes all fast cells (including 8.8 min inner ear) to off gas to a point that is below the natural background levels, and those fast cells will actually need to on gas upon reaching the surface to get back to normal levels. This means that the inner ear tissue gradient is now negative too.


It would seem the hypothesis in the paper above, regarding supersaturation and arterialized VGE and the overlapping period, does not apply to tech / deco diving, as the supersaturation conditions in the inner ear are no longer present upon surfacing.


Would you agree that this paper does not apply to the conditions of tech / deco diving?


.

 

[David Doolette]

I make exactly this point in the discussion following Simon and my paper in the Patent foramen ovale and fitness to dive consensus workshop, that appropriately timed decompression stops should reduce the risk of inner ear DCS (which is almost saying the obvious) by preventing an overlap of supersaturation and VGE - the relevant conditions are unlikely upon surfacing from a decompression dive, and that this might be one mechanism by which "safety stops" in recreational diving are useful. This is consistent with my own experience where I have seen more rapid onset CNS DCS following no-stop dives than following decompression dives. This is part of the reason I believe PFO pre-screening of technical diving candidates is a bad idea. This does not mean the same mechanism might not be relevant earlier in the ascent where inner ear DCS characteristically occurs in decompression diving. I review several potential mechanisms in the technical diving context in Diving Hyperbaric Med 2013;43:96-104.

David Doolette

 

[David Doolette]

Hi David, thank you very much for all your contributions to the discussion. I understand that a prophylactic closure of a PFO presents real risks, but wouldn't being screened for it and knowing whether or not you have one be at least of value for determining one's deco practices regarding things like physical regimen and computer conservatism?

My comment were only in the context of using pre-screening for PFO to make a decision about closure, and particularly where this was some sort of policy as a gateway to diving. If an individual wanted the information themselves, I would suggest that they have a defined plan of how they would deal with the result before a test.

David Doolette

 

[rjack]

My comment were only in the context of using pre-screening for PFO to make a decision about closure, and particularly where this was some sort of policy as a gateway to diving. If an individual wanted the information themselves, I would suggest that they have a defined plan of how they would deal with the result before a test.

David Doolette

I have heard the concept of coming up with a plan for PFO test results for a decade plus now (at least since I was bent in ~2006 and subsequently screened for a PFO). But I have never seen an example plan in all that time. A few things I can think of that PFO positive diver might decide to do are:
1) quit diving
2) quit technical diving
3) quit technical diving, continue recreational diving but use nitrox with air tables
4) change deco software or change conservatism of settings
5) add arbitrary conservatism (e.g. 10 more minutes on every dive at 3-6m)
6) add or change deco gases (e.g. adding EAN50 or O2 to a plan where in the past only 1 deco gas was used but keeping the stop times the same)

Are there options I'm missing? If you know of a thread or discussion someplace addressing what a "PFO plan" actually is and includes I would love to see it.

Richard

 

[Simon Mitchell]

Hello Richard,

Sorry, long post, but this is a complex issue. I will get to your specific questions about a “plan” in a moment.

First I want to address the advocacy for screening of all prospective technical divers for a PFO. At a very superficial level, the idea has some appeal, but if one digs a little deeper into the concept its flaws become apparent.

First, while serious neurological DCS remains an important concern for us, the fact remains that it is still a relatively uncommon event. Thus, the diving medical community has had to weigh the risks and benefits of invoking a screening program that involves an expensive invasive test with some risks, to find a lesion whose repair involves a very invasive procedure with substantial risks, in order to reduce the risk of an uncommon (albeit serious) event. It is a complex nuanced evaluation, but the consensus of experts is that the benefits of screening do not outweigh the likely risks. Some of the discussion below might help in understanding this judgement.

Even if we thought it might be a good idea, the complexity of invoking a widespread screening strategy should not be underestimated. For example, we have good evidence that large spontaneously shunting PFOs definitely increase the risk of DCS whereas small PFOs which shunt minimally despite provocation don’t. What we lack is a clear appreciation of the significance of the many lesions that lie between these extremes. Advising divers with such PFOs is a significant challenge. So, if we were running screening prior to starting technical diving, where would the cut-off be? All PFOs (which would be 30% of all those screened?) or just the large ones? This question is further complicated by the fact that the assessed “size” can be very dependent on the echo / bubble contrast / provocation technique used, and the experience of the interventionalist performing the test. You get the problem I’m sure.

The risk vs benefit discussion goes beyond the issues of testing / repair vs DCS for the individual. There is also a massive risk to the diving community / industry. For example, it is likely that given the difficulty in differentiating the risk associated with PFOs of different apparent size (as mentioned above), all PFOs (both large and small) would end up being treated the same by “officialdom” who tend to favour conservatism. Thus, it is likely 30% of all candidates would be excluded or forced to undergo repair.

In a related vein, it is also extremely unlikely that the medical community could justify a position that required widespread pre-participation screening for technical divers but not “non-technical” recreational divers (and that is another boundary that lacks a clear definition). As has been mentioned by David, PFO is very strongly associated with inner ear DCS arising from air dives at the deeper (30 - 40m) end of the recreational spectrum. So, if it was considered necessary to screen prospective “technical divers” it would be hard to argue that it is not necessary to screen all prospective divers. If that notion ever gained traction, then you could kiss goodbye to the diving industry overnight. Advocates of pre-participation screening need to be careful what they wish for.

Another plausible complication of a widespread screening program is the personal health administrative implications of widespread testing. For example, candidates who were positive and elected not to go technical diving might find other areas of their life complicated by the positive diagnosis. There might be problems with life insurance, travel insurance, or diving insurance if they wanted to continue recreational diving. There might be problems with career choices such as occupational diving, military diving, military aviation and others. Once problems like this started to emerge, it would deter at least some candidates from wanting to be tested in order to progress to technical diving.

None of this means that there is no path for an individual properly informed individual diver choosing to be tested. This pathway clearly exists and I have guided many people down it. But the complexities of this process must be understood by the diver and this is, at least in part, what David was referring to in relation to a PFO plan. The individual diver requesting testing for a PFO needs to be clearly informed about many things. I treat those things under 3 headings.

1. The implications of having the test.

I tell the diver that:

If they have the test there is at least a 30% chance of it being positive. If that happens, they are going to have to make some difficult decisions.

If the test is positive in the context of a previous episode of DCS, it does not guarantee that the PFO was the explanation for the DCS.

As a corollary to the above, if the test is positive and they have a PFO repair, it does not guarantee that the DCS will not occur again.

If the test is negative, it does not mean that they are somehow resistant to DCS.

If the test is positive, then there may be health implications outside the context of diving (which I have alluded to above).

If the test is positive then they have several options (see below) and if they are not interested in taking one of them, there is little point in having the test.

2. The risks of the test.

This is not a particularly big deal, but they do need to understand that they are going to have thousands of tiny bubbles injected into a vein, and if the test is positive, many of these bubbles are going to get into the arterial system. There have occasionally been transient neurological symptoms as a result and one or two of these have produced more lasting complications.

3. Choices if the test is positive.

If the test is positive, particularly if the PFO shunts readily, then the diver has 3 fundamental choices.

- give up diving

- dive in a manner designed to produce less VGE and avoid activities that would provoke shunting of VGE

- have the PFO repaired.

The second option (to dive in a manner likely to produce less VGE) is the focus of Richard’s attention on a PFO plan. He has identified a number of the options like: padding shallow oxygen stops, diving nitrox on air tables, adding conservatism to the chosen decompression algorithm, avoiding algorithms that appear to produce more VGE, reducing numbers of repetitive dives in a day, trying to maintain stable temperature profiles, use of strategies to avoid hard work during the bottom phase of the dive (like a DPV), maintaining sensible hydration, gentle exercise during decompression etc. Some of these are evidence based and some are somewhat speculative. And then there are strategies to reduce the likelihood of shunting bubbles after a dive, like avoiding hard work after a dive, particularly lifting or straining for 3 or 4 hours after surfacing.

This post is already long enough, but I hope I have illustrated how widespread screening is not as simple an issue as it may seem on first consideration. I will not discuss repair (and its risks) here, however there is one point I would like to emphasise. Even if we excluded every diver with a PFO, or repaired all the PFOs, it would not mean we no longer have to be worried about numbers of VGE. VGE can also cross pulmonary shunts which are potentially present in everyone, and they may cause adverse inflammatory responses in the absence of shunting to the arterial circulation merely because of their presence in the blood (though we are not certain of the significance of such responses). Pragmatic strategies to minimise VGE numbers will always be a legitimate goal of dive planning and decompression planning.

Simon M

 

[rossh]

I have heard the concept of coming up with a plan for PFO test results for a decade plus now (at least since I was bent in ~2006 and subsequently screened for a PFO). But I have never seen an example plan in all that time. A few things I can think of that PFO positive diver might decide to do are:
1) quit diving
2) quit technical diving
3) quit technical diving, continue recreational diving but use nitrox with air tables
4) change deco software or change conservatism of settings
5) add arbitrary conservatism (e.g. 10 more minutes on every dive at 3-6m)
6) add or change deco gases (e.g. adding EAN50 or O2 to a plan where in the past only 1 deco gas was used but keeping the stop times the same)

Are there options I'm missing? If you know of a thread or discussion someplace addressing what a "PFO plan" actually is and includes I would love to see it.

Richard

Looking back through this paper, DAN: Patent Foramen Ovale and Fitness to Dive Consensus Workshop Proceedings June 17, 2015 Montreal, Canada link

Page 47...

We see that a small diver PFO screening program was already carried out (10 years ago) by DAN Europe. It was part of a bigger test, and the screening part was deemed accurate. The conclusion was that the recreational diver need not be screened, but what about the high risk tech divers? We are 5x more likely to suffer DCS than a recreational diver, and a large portion of our injury cause can be attributed to RLS / PFO.

They screened for the bypass at the Carotid artery (neck) with a Doppler meter - easy.

There are numerous papers on RLS screening techniques, including trans-cranial, and carotid artery screening methods. Some of these are used on stroke patient testing now.

I would add, that the technician administering the procedure, doesn't need to be able to read the result, as it can be sent (internet) to DAN to be read and uniformly interpreted.

.

 

[rjack]

Thank you for the more nuanced thoughts on widespread screening.

And then there are strategies to reduce the likelihood of shunting bubbles after a dive, like avoiding hard work after a dive, particularly lifting or straining for 3 or 4 hours after surfacing.

This quote I assume is strictly in relation to PFOs, and at least for myself somewhat rare (to avoid lifting for that long). Are there any differences or unique considerations for pulmonary shunts? There has been considerable debate over the years about TEE and TTE echos for detecting PFOs and I imagine at least a few negative testing people actually have a pulmonary shunt despite being PFO negative. In my case I had a transcranial Doppler which in theory would detect a large pulmonary shunt, but I suspect the injected bubble load is way too small to detect pulmonary shunts reliably.

 

[Simon Mitchell]

Ross,

I guess you didn't read my post.

high risk tech divers?

Define "high risk tech divers". Do you mean all tech divers, and what is a tech diver? Or do you mean just some tech divers undertaking high risk activities, or what, exactly? How are you going to define your population for screening?

We are 5x more likely to suffer DCS than a recreational diver

Well, this is a bit of a revelation from you given that you have devoted considerable energy over a long time now trying to say that tech diving DCS rates have been plummeting along with everyone else.

Leaving that aside, and notwithstanding the difficulties both in defining "we", and the lack of accurate data describing rates of DCS, let alone relative rates, I agree that the poorly defined group known as "tech divers" are at higher risk of DCS (and based on personal observation of unreported events I think that rates of milder forms are grossly under estimated). But the fact remains that in the opinion of the medical community the rate of serious neurological DCS with permanent sequelae remains lower than needed to justify a prospective universal screening program prior to entry to tech diving (with all the difficulties that would bring as I described above). Equally, the community provides a pathway for properly counselled individuals to pursue testing if, after a very careful consideration of the risks and benefits of proceeding, they decide that they want to. This is the scenario considered most acceptable by the medical community.

They screened for the bypass at the Carotid artery (neck) with a Doppler meter - easy.

This method still requires the use of bubble contrast and is no more benign. Moreover, all it does is identify the presence of a right to left shunt. It cannot distinguish between a PFO or a pulmonary shunt. Anyone who has a positive test done with carotid Doppler will need to go on and have another test with echocardiography to characterise the lesion. For this and other reasons, it is not considered a good tool for use in clinical evaluation of divers (it may have a place in some types of research). The two contemporary consensus statements on the matter clearly identify transthoracic echo with bubble contrast and provocative manoeuvres as the standard.

SMART D, MITCHELL SJ, WILMSHURST P, TURNER M, BANHAM N. Joint position statement on persistent (patent) foramen ovale and diving. South Pacific Underwater Medicine Society (SPUMS) and the United Kingdom Sports Diving Medical Committee (UKSDMC). Diving Hyperbaric Med. 45, 129-131, 2015.

MOON RE, MITCHELL SJ, BOVE AA. PFO statement. In: Denoble PJ, Holm JR (Editors). Patent Foramen Ovale and Fitness to Dive Consensus Workshop Proceedings. Durham, NC, Divers Alert Network, 141-144, 2016

I would add, that the technician administering the procedure, doesn't need to be able to read the result, as it can be sent (internet) to DAN to be read and uniformly interpreted.

At a practical level this is rubbish. DAN does not offer a service for interpretation of bubble contrast echo that could be used as part of a widespread screening program. This is another example of you commenting authoritatively on complex medical matters that you have no knowledge of. Debates with me would be a lot less frequent if you refrained from doing this. When performing a bubble contrast echo the best accuracy (especially for the less obvious lesions) is obtained when the senior proceduralist is in the room to supervise the imaging, the precise timing of bubble contrast administration, the timing and nature of provocative manoeuvres, and to see the images in real time. There is no doubt that a senior experienced echo-sonographer could also do a good job of this, but it is not as simple as you portray it, and they would want to do it in real time also. In many jurisdictions, bubble contrast use requires the presence of a medical proceduralist like a cardiologist. Just in case you intend questioning it, I am not a cardiologist, but trained as a cardiac anaesthesiologist and in the use of echocardiography.

Simon M

 

[Simon Mitchell]

This quote I assume is strictly in relation to PFOs, and at least for myself somewhat rare (to avoid lifting for that long). Are there any differences or unique considerations for pulmonary shunts? There has been considerable debate over the years about TEE and TTE echos for detecting PFOs and I imagine at least a few negative testing people actually have a pulmonary shunt despite being PFO negative. In my case I had a transcranial Doppler which in theory would detect a large pulmonary shunt, but I suspect the injected bubble load is way too small to detect pulmonary shunts reliably.

Hello Richard.

One of the problems with testing for pulmonary shunts is that they are not as easy to provoke into shunting as a PFO. There is some evidence that that rate is close to zero at rest (the conditions of PFO tests), but rises considerably during exercise (up to 90% of subjects in at least one study). In fact, the safest assumption (and probably an accurate one) is that the vast majority of us are capable of shunting across the pulmonary circulation under the right circumstances. The avoidance of exercise, lifting and straining, etc after diving is also just as relevant to pulmonary shunts, so even if you don't have a PFO, it is probably best to minimise those things as much as is practicable after diving.

Hope this helps.

Simon M