PFO story

This is my story of being diagnosed with a Patent Foramen Ovale (PFO) and learning about diving medicine that isn't covered in the usual courses for divers.


Contents:


Patent Foramen Ovale

Summary

A patent foramen ovale is a type of opening in an internal wall of the heart. It is quite common. It usually has little significance in ordinary life, but is dangerous for divers.

Where it comes from

In normal adults, the veins carry `used' blood into the right side of the heart, where it gets pumped out into the lungs, picks up oxygen, comes back to the left side of the heart, and gets pumped out again into the arteries. However the unborn foetus is different, because it does not breathe air. To save energy the foetal heart does not pump blood unnecessarily through the lungs; instead it lets most of the blood pass through an opening called the foramen ovale (`oval window') in the wall between the right and left atria (collecting chambers) of the heart.

At birth the heart must suddenly switch over to pumping all blood through the lungs. To achieve this, the heart wall grows a flap of tissue capable of sealing the opening, on the left (downstream) side of the wall. In the foetus this flap is pushed away from the opening by the stronger pressure on the right (upstream) side of the heart. At birth, the baby's first breath causes a back-pressure to build up in the vessels supplying the lungs; the pressure in the left side of the heart pushes the flap closed; and blood starts to circulate through the lungs.

In three-quarters of adults this flap has grown completely closed over the foramen ovale and the opening is sealed. However in about one-quarter of adults it does not seal completely and remains open or capable of opening ("patent") to some extent. This is a patent foramen ovale.

The size and "patency" of the opening vary widely in the population. The distribution of sizes is very skewed to the right: most people who have a PFO have a very small one, but there are a few very large extremes. Most often the PFO is just "probe patent", meaning that a ballpoint-sized probe could be pushed through it. At the other extreme there may be an unprotected hole as much as 4-6 cm in diameter.

Read this general description of a PFO for medical practitioners.

What it means for your ordinary life

The short answer is: "nothing", unless we are talking about a very patent one.

It seems to be universally agreed by doctors that a PFO has no clinical significance, unless it is so patent as to cause a large fraction of blood to be `shunted' across the opening, bypassing the lungs. People with a very patent PFO are usually very sick from their childhood onward until/unless the opening is closed by surgery.

However, you can have quite a large PFO without knowing it. For the majority of people with a PFO, the opening only allows blood to pass through under certain conditions where the pressure is transiently higher on the right side (coughing, straining, Valsalva manoueuvre) and then only a small amount of blood is involved. Hence oxygen supply is not compromised and there is no impairment of fitness.

Statistics show that PFO's (of all sizes, lumped together into one category) are very slightly associated with shorter life expectancy, cryptogenic strokes, thromboembolism and other accidents. A possible explanation is that an object such as a blood clot is able to pass through the PFO into the arteries where it could cause damage by blocking blood flow to the brain, etc. Of course these statistics could just be a reflection of the extreme cases [a good example of a random effect]; it might only be the very large ones which are dangerous. The estimated absolute risks are very small numbers.

Here are some references from MedLine.

What it means for divers

It means "bubble trouble": a PFO can cause decompression sickness or arterial gas embolism. Read the article in Diving Medicine Online:
In divers there is the risk of paradoxical embolism of gas bubbles (passage of bubbles into the arterial circulation) which occur in just about all divers in the venous circulation during decompression. Blood can flow in both directions with intra-atrial shunts at various phases of the cardiac cycle and some experts feel that a large atrial septal defect (PFO) is a contra-indication to diving. In addition, a Valsalva maneuver, used by most divers to equalize their ears during descents and ascents, can increase venous atrial pressure to the point that it forces blood containing bubbles across the PFO into the arterial circulation. Thus the usual filtering process of the lungs is by-passed.

Statistics show pretty unequivocally that divers with a PFO have a higher risk of DCS. The mechanism (hypothesised) is that bubbles of nitrogen in the blood, which form in the veins of every diver during a dive, can pass from the veins through the PFO into the arteries, instead of going to the lungs where they would be filtered out. Bubbles in the arteries can go anywhere and cause gas embolism (blockage of blood flow) particularly in the brain.

There must be a lot of divers who have a PFO - perhaps 10-30% of the diving population. Obviously not all of them have had decompression sickness. One possible reason is that PFO's vary widely across the population and the vast majority of them are quite small. Therefore a PFO is not in itself an exclusion to diving. The Australian Standard for assessing fitness to dive does not list PFO as an exclusion.

However if a diver has had decompression sickness and is found to have a PFO, many experts believe the DCS is probably attributable to the PFO.

If a diver suffers decompression sickness in an otherwise uneventful dive, it is prudent to check whether the diver has a patent foramen ovale. If it then turns out that you do have a PFO, most doctors will strongly recommend that you cease diving altogether. The combination of a history of presumed DCS and a diagnosed PFO would probably be enough for certification agencies to decline to certify someone for any new courses.

Surgical closure of PFO

There is a God! (..... Neptune!)

There is a prospect of having the PFO closed by surgery. The latest procedure is superficially similar to angioplasty. It uses a catheter inserted through a large vein in the groin. A tiny disc of titanium-nickel mesh (or a similar arrangement) is fed through the catheter into the right atrium, fastened over the hole, and the catheter withdrawn. The heart wall tissue grows over the discs. The operation takes about an hour and you can walk out of hospital within a day. [So say the internet promo pages....] There are several devices for closing PFO's and other atrial septal defects. Apparently the only device available in Australia is the Amplatzer® Septal Occluder.

Here are

These procedures are not without risk. However they have been performed on thousands of children with large life-threatening PFO's. The application to divers has been led by Dr Peter Wilmshurst and colleagues in the UK. See his announcement in Diver, February 1997 referring to an article in The Lancet, 14 September 1996, page 752. Several divers have had large PFOs closed and have returned to diving!!!

Many doctors regard these procedures as too risky to undertake unless you really need it to safeguard your life. ["He must be mad", said one, "take up sky diving", etc etc. ] In a recent trial of several such devices, the operations had a success rate of 98% and a complication rate of 5-10% (some nasty complications too); the surgeons were "on a learning curve" with the devices used. Anyway it's still heart surgery; for example there are higher long term risks of infection, etc. with a foreign body in the heart. So, perhaps it's not a magic wand.

Current opinion seems to be that the closure operation would be justified for a professional diver. Some doctors would say the closure operation may be justified for a recreational diver whose wish to continue diving is so strong that to stop diving would severely affect their personal life.

My case

April 2000: I'm an enthusiastic diver, 120 dives in 2 years, PADI Rescue certification. I dive with a computer, I'm getting very economical with air, and regularly go to the edge of the PADI Tables (group W-X) and sometimes beyond. My last two dives were: 18 metres for 47 minutes, surface interval 2 hours, then 15 metres for 61 minutes (bottom times). That is about the most extreme exposure I've had, and I've never had any problems before. OK, I admit this was pushing the limits.

In January 2000 I had a persistent feeling of light-headedness and disorientation, and an inability to concentrate. It didn't seem related to my diving. It continued for several months.

I went to my GP, who found nothing significant, but sent me for blood tests and a CAT scan of the head. I also consulted the Diving Medical Service, 135 Dunedin St, Mt Hawthorn WA 6016, phone 9444-8977. Dr Greg Deleuil was very thorough, read my log book, thought the symptoms were vaguely indicative of DCS, and recommended I front up to the Hyperbaric Unit, Fremantle hospital, phone 9423 2233. The staff there were also outstanding -- careful, professional, dedicated and considerate --- especially Dr David Wright. Dr Wright conducted a standard battery of neuro tests, with no striking results but some sluggishness. They chucked me in the recompression chamber (Royal Navy Table 62, maximum `depth' 18 metres, total time 5 hours) and after 45 minutes my sense of well-being and concentration seemed to improve suddenly, although subtly. So the diagnosis was DCS.

[Postscript: My ability to concentrate suddenly returned to normal about the end of June. Only then did I realise just how bad it had been. Suddenly I could concentrate for 4 hours without looking up, instead of wandering after 2 minutes.]

Dr Wright explained that neurological DCS processes can include an inflammatory response with symptoms similar to an infection and/or subtle impairment of function. A theory is that white blood cells are mobilised into the small blood vessels that have suffered trauma, resulting in decreased flow through those vessels. The symptoms can be vague and persistent. Recompression works not only because "the bubbles are squashed again" but also because hyperbaric O2 has pharmacological effects which help to suppress the inflammatory response.

At this stage Dr Wright referred me to cardiologist Dr Phillip Currie, Echo Services, an expert in echocardiography (again a privilege to be able to consult some top people). The standard diagnostic test for a PFO is a bubble contrast echocardiogram. An ultrasound transducer is placed against your chest. Some of your own blood is extracted, mixed with saline solution, agitated to make bubbles (which can be seen on the echo image), and reinjected. Then you are asked to do a strong Valsalva manoeuvre (in my case, just to take a deep breath and bear down on it).

Sure enough, there was the picture I did not want to see - a shower of bubbles entering the left atrium, betraying the presence of a PFO.

I was counselled by several doctors that the best option was to give up diving. I expressed a stubborn determination not to take this lying down, spent a lot of time in the Medical Library, and was probably a difficult patient.

I was advised that if I really really want to continue diving (furious nodding here) I could minimise my risk by avoiding repetitive dives (i.e. only 1 dive in a 24 hour period), keeping the ascent rate below 3 metres/minute, limiting depth to a maximum of 18 metres, and having very conservative bottom times. However any recurrence of DCI under these conditions would lead to very emphatic advice to stop diving.

I was referred to cardiologist Dr Paul Langton (via Echo Services) for further consultation. Dr Langton is also an expert in hyperbaric medicine and a member of SPUMS. It was a privilege to meet him and I'm immensely grateful for his help. Dr Langton gave me a searching examination, consulted numerous experts on my behalf, and gave me very detailed advice. I would highly recommend any divers out there with similar problems consult him.

Dr Langton referred me for additional tests including a transoesophageal echocardiogram (a transducer down the throat to get closer to the heart) and an MRI scan of the heart. These gave good clear pictures of the anatomy of the PFO and determined that it is about 1 cm across, and passes the criteria for the closure procedure. After some consideration (ooooh... at least 3 minutes!) I decided to ask for the closure operation.

The operation was performed by interventional cardiologist Dr Bernard Hockings. It was such a privilege to have the help and kind support of Dr Hockings, and the team at the Charles Gairdner Hospital. The day I went in for surgery the cardiac ward was completely full and I felt very humble to be allowed to slip in between the crisis cases. The operation itself took less than an hour and was virtually painless. (The hardest thing is lying motionless for the next 6 hours while the anticoagulant wears off.) The next day an echocardiogram, to check that the device was in position, and I walked out of hospital! (slowly)

A fortnight later, another echocardiogram to verify that the device was still in position. Dr Hockings explained that the heart wall has repair cells that detect the device and extend pseudopoda over the struts. After two-three weeks there is a one-cell-thick layer covering the device (at which point the risk of infection is decreased), and after two months the connective tissue has completely filled the spaces in the device and it becomes invisible to ultrasound.

It was decided that after three months I could return to diving!!

I made a couple of very gentle dives (in the pool and the jetty at PDA in Fremantle) with no trouble, then gradually extended the range. I took a basic Nitrox course to improve my safety on ordinary recreational dives. I'm now back to diving in earnest.

(Postscript, Oct 2002: I'm still diving. Since the operation I have dived over 200 times, including a chamber dive to 50 m and air decompression dives to 40 m, with no ill effects. I've done more courses to improve my skills and safety, and carefully extend my diving limits: PADI Wreck, PADI Deep, TDI/SDI Advanced Nitrox, TDI/SDI Decompression, PADI Drysuit. )

(Postscript, Dec 2004: I have now dived over 500 times since the operation, including dives in strenuous conditions such as strong currents and hard surface swimming. I have also learned to dive on a semiclosed rebreather, in which the diver inhales and exhales against a substantial pressure differential, unlike open circuit scuba. I have had no ill effects.)

Statistical comments

Here are some thoughts about the statistical interpretation (for anyone who is still listening).

Studies have estimated the risk of DCS at 0.05% per dive in the overall diving population, and perhaps 0.3% per dive for divers with a PFO. In 100 dives that would mean a DCS probability of about 5% and 25% respectively, under some assumptions. (Must remember to use that as an example in Statistics 101).

When a diver who has had DCS is diagnosed with a PFO, medical advice is

  1. give up diving because the PFO and other factors are obviously [medically] significant enough to have caused DCS;
  2. a PFO is "not very [clinically] significant" for your health in ordinary life.
Point 1 is a valid use of Bayes' theorem (in anyone's theory of inference) based on observational studies of divers with DCS (contingency tables with sample sizes up to about 100). Point 2 is based directly on observed frequencies in large epidemiological studies, and is fairly sound. Both points are (probably) statistically valid advice given only the yes/no information that the patient has a PFO (yes/no) and a history of DCS (yes/no).

What seems to be missing is a measure of degree (e.g. severity of the DCS, size of PFO, dive exposure) in assessing the medical history. It's a classic example of a random effect. After all, "I" want to gather all available information to weigh up "my" personal risk of illness in ordinary life with the PFO (e.g. the conjectured elevated risk of stroke), "my" personal risk of DCS while diving with the PFO, and the risks if "I" were to have surgery to close the PFO. (Is this a version of "hell for statisticians"?) This information is apparently not available about the population broken down by size of PFO. To my way of thinking it is an open question whether a PFO of a given size should be considered clinically significant. There is insufficient objective basis (from population studies) for such decisions. Still it would seem prudent in each case to investigate the anatomy of the PFO and make whatever clinical judgements can be made with this extra information.


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