Patent Foramen Ovale

[The Iceni]

This is a quote from the BSAC site.

"A year ago I was treated for DCI . I developed symptoms 30 hours after diving - (my buddy developed symptoms within in 45 minutes). I decided to take a year out from diving and within that year my medical has expired. I would like to start diving again but want to limit myself to 20m.

As I answered YES to the DCI question on the self certification form I needed to refer myself to my area medical referee. He will not see me until I have a PFO test. My doctor has deemed this as non essential (so is not avaliable free on the NHS) and I will need to pay approx £340 to have this test.

For my own peace of mind I would like to have this test too. Does anyone know of how to get a PFO test cheaper than £340 or is this going rate ?

I am based in the North East."

I replied as follows.

"I find this story extremely disturbing. Was the diagnosis confirmed and were you treated for DCI, at a recognised hyperbaric unit? If your buddy developed symptoms within forty five minutes he should have been treated and in my professional opinion you most certainly should have been in the chamber with him. As you developed symtoms after 30 hours quite clearly you were not.

This seems to be a bit of a conundrum does it not? IMPO if the presence of a PFO is significant the doctors at the hyperbaric chamber in which you (and your buddy) were treated should have excluded a PFO as a part of the work up on you.

What concerns me most is that if BOTH you and your buddy had a hit it is more likely that (statistically at least) you were just unfortunate, as DCI happens. The obvious alternative is that you both have left-to-right shunts and your buddy's is larger than your own.

DCI happens whether a PFO is present or not but I understand a PFO is thought to be present in 30 percent of the general population (and therefore by extension in the same proportion of divers) but it is the size of this shunt that is the important feature for DCI. If you both are experienced divers, particularly with many deco dives I think it is very, very unlikely indeed that a shunt is the main cause of your problem.

On the other hand if these hits were experienced on your first long or "technical" dive - where microbubbles are a constant feature in the veinous system - the presence of a shunt is much more likely but not guaranteed.

I would be a little concerned if what you imply is correct;

My understanding of what you say is as follows.

Divers who have had a DCI will not now be allowed to dive again until a PFO has been excluded even if the doctors who provided treatment of the original incident did not consider a PFO to be a potential cause and did not look for it.

Personally, I do not see how any patient can ethically be forced to pay for a further investigation if the doctors caring for him/her failed to perform that particular investigation at the time of initial treatment, whether this was because they did not condsider it necessary (or probably more importantly, if they were negligent.)
I would be very interested to learn the full details of this case."

I have since learned that this was a w/e trip consisting of five no-stop air dives all at about the 30 M mark so I suspect Peter and his Buddy were just unlucky. He admitted to being dehydrated (a lesson for us all).

In these litiginous times I just wonder if his medical referee is right to refuse a certificate of fitness without a risky and expensive PFO test when I suspect dehydration must have been the cause of this incident.

Any thoughts?

 

[DocVikingo]

Hi Dr. Thomas,

Perhaps such matters are handled differently in England. However, based on US practices, and the incomplete information provided by the poster (e.g., dive conditions, specific signs & symptoms), yes, I do have a number of issues & thoughts.

1. The opinion that, "If your buddy developed symptoms within forty five minutes he should have been treated and in my professional opinion you most certainly should have been in the chamber with him. As you developed symptoms after 30 hours quite clearly you were not."

I agree that the buddy was a candidate for hyperbaric attention. However, it is not my understanding of current chamber practices that the poster routinely would have been treated.

Is it your understanding that a hyperbaric facility is obligated to customarily treat the buddy of a bent diver who has no signs or symptoms of DCS [and/or provides no history of a very worrisome dive profile, e.g., missed deco requirements]?

2. The opinion that, "IMPO if the presence of a PFO is significant the doctors at the hyperbaric chamber in which you (and your buddy) were treated should have excluded a PFO as a part of the work up on you."

Even assuming that the expertise & equipment needed to do such a work up were on-site, in the absence of particular features, e.g., a suggestive clinical picture or history, unexplained episode of DCS, Type II DCS, I doubt that the hyperbaric facility is legally remiss in not seeking to exclude PFO as a matter of course, whether this be done on-site or through a recommended post-treatment cardiac consultation.

I also would be surprized if insurers would cover the expense of such a diagnostic pursuit on a routine basis. Apparently the poster's physician did not find it appropriate for coverage under the national health system. Although this chap's medical referee has reportedly made such r/o a condition of return to diving, and the odd outlying physician recommends that all potential divers be evaluated for PFO before seeking certification, I am not aware that this is the standard of practice without such specific reasons as discussed above. I could be mistaken.

3. The statement, "What concerns me most is that if BOTH you and your buddy had a hit it is more likely that (statistically at least) you were just unfortunate, as DCI happens. The obvious alternative is that you both have left-to-right shunts and your buddy's is larger than your own."

While DCS does happen, and can be unexpected, it's statistical rarity in the presence of safely executed recreational profiles leads me to opine that if both divers were in fact bent then it's more likely that they both engaged in a dive(s) that predisposed to DCS rather than that they were "just unfortunate." The DCS may have resulted from time at depth or other conditions like cold, heavy exertion, dehydration or a combination of factors.

It later came to light that this poster was on a "w/e trip consisting of five no-stop air dives all at about the 30 M mark," and this led you to "suspect Peter and his Buddy were just unlucky." Even leaving aside such unreported upon items as the extent to which NDLs were pushed, dive conditions, ascent rates & safety stop parameters, I believe it could reasonably be argued that 5 dives all to a depth of around 30M/98' constitutes not the most conservative of two day scuba outings for a diver who admits to being less than optimally hydrated.

Moving on to your next sentence. PFO is an atrial septal defect of a type that blood can routinely shunt in either direction, although left-to-right is the predominant state with right-to-left leakage typically small. However, it's when blood flows from right-to-left, which can occur with the boost in venous atrial pressure occasioned by equalization techniques like the Valsalva maneuver, that bubbles can pass directly into arterial circulation and become a serious problem.

4. The remark, "...a risky and expensive PFO test...."

It is my understanding that the most commonly used techniques are:

a. Transthoracic echocardiography (TTE), which is essentially risk-free.

b. If TTE proves inconclusive, or even as an initial procedure, transesophageal echocardiography (TEE) may be performed. This is a more sensitive technique with a mildly invasive aspect that has a low reported incidence of significant complications. Those undergoing TEE often have sore throats for a few days, but serious complications such as perforation of the esophagus or material bleeding apparently are only quite rarely reported.

Riskier techniques, like heart catheterization, seem to be infrequently used and reserved for special situations.

I have only a vague idea of the cost of such procedures, with TEE obviously being the more expensive. However, I suspect that TTE is about mid-range in the gamut of modern imaging techniques, which is not to say it's inexpensive.

Best regards.

DocVikingo

 

[The Iceni]

Thanks VK

As I undesrand it these things aren't handled very differently over here.

1) I am not active in hyperbaric medicine but it would seem sensible to have treated both as their reported dive profile(s) may not accord with reality. They both had the same profiles and one diver suffered DCI, which could not be attributed to any shunt with any degree of confidence at the time of treatment.

2) I completely agree that the hyperbaric facility has no requirement to exclude PFO as a matter of course. This leads me to question why the medical referee has made this test a condition of a return to diving

3) I agree, its is far more likely that they both engaged in a dive(s) that predisposed to DCS rather than that they were "just unfortunate" as they admitted to being less than optimally hydrated and in addition were not "dived up".

4) I suspect his buddy may have a shunt but doubt the poster has because there were other sufficient predisposing factors. (As you say luck doesn't enter into it.)

The poster has a problem.

If he wishes to continue to dive BSAC it seems he must pay over £400 to exclude a condition for which there is little clinical evidence. OK, Dr VK, what if he has a TEE and this excludes or confirms a small shunt? He has already stated that his future diving will be more conservative, less than 20 M and he will watch his hydration status.

It would seem to me that as the poster is doing all that is required already, in my opinion the referee's decision, to insist on a PFO test is not really justified but perhaps the diver should be "medically downgraded" at least temporarily, rather than banned in any case?

 

[Hobbs]

I have a question,
I am not in anyway a doctor or medical person what so ever, but
I am a diver and as such interested in the dangers we face.

This person that is under discussion have he had DCI type 2 ? since if I am not mistaken that would be the only time when a PFO even can be considered to be "cause/contributor to the problem", if it was a type 1 then there is no relevance to the PFO
wich then would make it irrelevant to test for PFO
am I right ??

I am not saying that it is wrong to do the test, I just question why the test is required

Please correct me if I am wrong.
and if I am wrong can anyone please tell me the difference off type 1 and type 2 DCI couse somewhere I must have mixed it up then.

 

[DocVikingo]

Hello Hobbs,

Let's deal with terminology first. In essence, Type I DCS involves the joints, muscles, skin & lymphatics, while Type II involves the central nervous system & lungs.

It is not possible to determine if the divers in question sustained Type II DCS based on the material presented by Dr. Thomas. What is reported is that one member of the buddy pair was treated for DCS after developing features 45 minutes after the last dive, while the other was treated for features of DCS developing 30 hours after the last dive.

Type II DCS is one event that would make one look further into the possibility of PFO, but not the only one. An unexplained Type I DCS event, especially if recurrent, is another.

Hope you found this informative.

DocVikingo

 

[Stone]

How is "Patent Foramen Ovale" pronounced?

 

[BillP]

pay’-tent for-a’-men (long a) o-va’-lee (short a, kinda like O'valley)

Dr Thomas probably says it differently in his English English.

 

[The Iceni]

How about

Pay tent foray men ovaarlay?

Not strictly English English as it is Latin but my (English) Latin teacher insisted an "e" at the end of an adjectve in the possissive case is pronounced as a long "a".

and of course this all has to be spoken as if you have a hot potato in your mouth!

Goodness knows how my Latin teacher can claim to know how Latin was pronounced. I have not seen any Romans around these parts for a year or two!

On a more serous note. I am not so sure that distinguishing between type 1 and type 2 DCI is terribly helpful. As I understand it there is a spectrum and each case can be graded according to its speed of onset and affected tissue type.

A rapid onset CNS bend is much more serious and also likely to due to a shunt, particularly if the profile was reasonably conservative.

 

[DocVikingo]

Hi Dr. Thomas,

Sorry to be so delayed in this reply, but your industry is difficult to keep up with.

I'd like to comment on your remark, "I am not so sure that distinguishing between type 1 and type 2 DCI is terribly helpful. As I understand it there is a spectrum and each case can be graded according to its speed of onset and affected tissue type."

To the extent that the following may be construed as "helpful," to the best of my knowledge this distinction has a long & meaningful history both in the literature & in clinical practice. I do know that it continues to be applied in ongoing research on DCS by several major organizations. Finally, it most certainly is terribly helpful in as much as current US Navy recompression protocols for DCI are based on this distinction.

I do, however, agree that DCI is a spectrum of signs & symptoms that could be graded according to speed of onset & affected tissue type. It would be interesting to see such a spectrum nosology developed & correlated with treatment outcomes.

Best regards.

DocVikingo

 

[The Iceni]

Hi Dr Vikingo,

As you say, if the required treatment table obliges the attending physician to differentiate between type I and type II DCI it has obvious practical relevance and extreme importance.

As I am not in that type of practice the obvious implications were quite lost on me!

I suppose I have looked upon this as similar to treating asthma, where the tradititional two types of "intrinsic" and "extrinsic or atopic" asthma do not loom large in the algorithms employed in clinical practice, only the severity of the attack.

I presume there are three factors the hyperbaric physician must consider when deciding the necessary treatment.

1) the speed of onset of symptoms.

2) the severity of those symptoms.

3) the affected organs.

Extrapolating from this.

If 1 is rapid, 2 is severe and 3 is CNS or cardiopulmonary, more aggressive treatment is necessary, I suppose?

(learning all the time)