Patent foramen ovale

[steevke]

I'm scheduled to have my PFO closed in about 3 weeks. Does anyone out there have any idea what I should expect in the form of side effects? I've heard mirgraines might be an issue. Is there anything to that?

I've had an ASD closed last year, after an 'undeserved' pain only hit. I did not even know I had the defect. Funny thing is that after the operation I suddenly noticed I did not hear any 'murmum' anymore when sleeping

The actual procedure (in my case) was a breeze. Got in on sunday, and on monday afternoon they inserted an occluder (kind of like a double sided umbrella) through a catheder in the groin up into the heart. Then the occluder is opened up on both sides of the defect and then the wire is removed. This takes about 20 to 30 minutes and is done under general anaesthesia.

After the operation you have to lay absolutely still for 12 hours or so, you can't move, as you still have the catheder stuck in your vein - it hurts if you move. After that period, they remove the catheder, an extra x-ray is taken to make sure the device is still in place, and then you go home. 3 months later you get another TOE to check for residual shunting.

Staying still was the hardest part (for me).

Good luck with your operation.

Steven

 

[jknight]

I've had an ASD closed last year, after an 'undeserved' pain only hit. I did not even know I had the defect. Funny thing is that after the operation I suddenly noticed I did not hear any 'murmum' anymore when sleeping

Steve,
Thanks for the heads up. They might have to sedate me to keep me still for 12 hours.

Thanks again.
Jon

 

[The Iceni]

. . . This is actually the reason I don't believe it was an AGE at all. An AGE would definitely have been affected by recompression, and inversely, without hyperbaric oxygen, you probably wouldn't have survived at all ... So personally, I'd rule any form of DCI out at all ...

Hi Tom,

I can understand your point of view.

Let me try and explain mine a bit more. In clinical practice we see many, many patients suffering from paroxysmal thromboembolic events - or "strokes". These can range from a transient ischemic attack, which completely resolves within 24 hours (by definition), to an immediate fatality.

The degree of injury mostly depends on the size of the embolus and the degree of subsequent tissue hypoxia (ischemia).

So how large does a cerebral AGE have to be (or how many bubbles need to be arterialised to the cerebral capillary tree) before intracranial pressure is sufficiently increased or ischemia produced due to blockage of a major cerebral artery (as with thomboembolic strokes) to cause transient loss of consciousness on ascent for which no evidence exists on arrival in hospital or at post mortem?

I do not pretend to know the answer, but I bet it would not be huge and need not be produced by clinically obvious pulmonary baraotrauma. I would aver that it possible that this could be derived from a ruptured alveolar bullus delivering repetitive showers of very small bubbles at depth (in a smoker for example).

Sadly this is not something that could be the subject of an ethical clinical trial. Nor is it somthing the average pathologist will consider at post mortem as original cause of the incident; - "Drowning" is sufficient for the coroner.

Cerebral ischemia and raised intracranial pressure can both cause loss of consciousness.

Another point is that I do not believe that it is possible to survive so long without some ventilation at all. I have not had this confirmed by my rescuers but it is possible -even likely - that my regulator remained in my mouth with a very poor seal when unconscious to deliver sufficient oxygen for my survival.

 

[miguel sanz]

There are other causes of paroxysmal thromboembolic events than cardiac shunts: arterio-venous pulmonary shunts, that can also be present undiagnosed. Although far less frecuent than PFO. Other AGE could not be paroxysmal but from undiagnosed pulmonary barotrauma; also some people have little cysts on there lungs that won´t cause anyother problem.
Is that right?

 

[fins wake]

So how large does a cerebral AGE have to be (or how many bubbles need to be arterialised to the cerebral capillary tree) before intracranial pressure is sufficiently increased or ischemia produced due to blockage of a major cerebral artery (as with thomboembolic strokes) to cause transient loss of consciousness on ascent for which no evidence exists on arrival in hospital or at post mortem? I do not pretend to know the answer, but I bet it would not be huge and need not be produced by clinically obvious pulmonary baraotrauma. Cerebral ischemia and raised intracranial pressure can both cause loss of consciousness.

This is very interesting. What originally made me write my thoughts on the matter was a vague memory from a previous dive medic course about various prevalences of certain symtoms when AGE was suspected or (later) diagnosed. Unfortunately I can't find my course material right now, and hence the reference, but it was a UK study, probably RN. I seem to remember that clinically obvious pulmonary barotrauma was very prevalent, but even so that would not negate your observations. Fascinating stuff.

Another point is that I do not believe that it is possible to survive so long without some ventilation at all. I have not had this confirmed by my rescuers but it is possible -even likely - that my regulator remained in my mouth with a very poor seal when unconscious to deliver sufficient oxygen for my survival.

Yes, that's exactly what I think happened. Take a look at the discussion on the tragic Michael Norwood fatality at The Deco Stop, there are some possible similarities there. (Please note that all this is speculation.)

(Just for the record and to avoid misunderstandings, I am not Tom Mount [I wish!], but merely using a quote of his from another discussion as my tagline. He's a true dive legend. :lookaroun )

 

[ArcticDiver]

After reading this and other threads I'm left with a couple questions.

-While a TEE is the preferred diagnostic tool when looking specifically for a PFO would one be picked up on any other cardiac examination, invasive or otherwise?

-If repair is required what, if any, anti-rejection and/or anti-coagulant medications would be required? For what time period?

 

[DocVikingo]

(Q) While a TEE is the preferred diagnostic tool when looking specifically for a PFO would one be picked up on any other cardiac examination, invasive or otherwise?

(A) Patients with large PFOs may have a heart murmur. However, excluding echocardiography, on balance it's rather unlikely that anything will be picked other than perhaps on autopsy.

(Q) If repair is required what, if any, anti-rejection and/or anticoagulant medications would be required? For what time period?

(A) There are a couple of surgical procedures, primary closure where the hole is simply sutured & secondary closure where a tissue patch is placed, as well the non-surgical placement of an occlusive device via cardiac catheterization (preferred method when possible).

What technique is applied depends on how large the opening is & other factors. What medication(s) is used pre/post-procedure depends upon the technique performed, the patient's clinical picture & other factors.

Best regards.

DocVikingo

 

[The Iceni]

Hi Arctic Diver,

This is the occlusion device my cardiologist used. I doubt many defects found in adults would now be closed by a primary suture as this is "open heart surgery". (In paediatrics it is another matter entirely.)

As the device is made of inert material, as with hip replacements and artificial heart valves, there is no need for any antirejection therapy but there is a brief indication for anticogulation;-

As you can see from the link the device consists of two mesh "umbrellas" facing each other like a burger bun, which are placed each side of the defect. I was advised to take low dose aspirin (75mg daily) for six weeks to reduce the risk of a large clot forming on the left atrial surface (which could embolise and cause another stoke). During this time the mesh is gradually epitheliarised - it becomes covered in endothelium (skin if you like) and an integral part of the heart wall.

As DocVikingo says a PFO is seldom diagnosed in life because, in the general population at least, it is not pathological and causes no symptoms. Trans thoracic echo can also be used to demonstrate a defect. It is less invasive than TEE but is also less sensitive.

I understood DAN Europe were in the process of organising a trial of screening for PFO in sport divers using simple carotid doppler and bubble contrast.

Anyone know what became of that? I have been a bit out of touch.

 

[DocVikingo]

The DAN Europe study that you reference is ongoing.

Best regards.

DocVikingo

 

[ArcticDiver]

Hi Arctic Diver,

This is the occlusion device my cardiologist used. I doubt many defects found in adults would now be closed by a primary suture as this is "open heart surgery". (In paediatrics it is another matter entirely.)

As the device is made of inert material, as with hip replacements and artificial heart valves, there is no need for any antirejection therapy but there is a brief indication for anticogulation;-

As you can see from the link the device consists of two mesh "umbrellas" facing each other like a burger bun, which are place leach side of the defect. I was advised to take low dose aspirin (75mg daily) for six weeks to reduce the risk of a large clot forming on the left atrial surface (which could embolise and cause another stoke). During this time the mesh is gradually epitheliarised - it becomes covered in endothelium (skin if you like) and an integral part of the heart wall.

As DocVikingo says a PFO is seldom diagnosed in life because, in the general population at least, it is not pathological and causes no symptoms. Trans thoracic echo can also be used to demonstrate a defect. It is less invasive than TEE but is also less sensitive.

I understood DAN Europe were in the process of organising a trial of screening for PFO in sport divers using simple carotid doppler and bubble contrast.

Anyone know what became of that? I have been a bit out of touch.

Thanks for the information. I was familiar with the generalities but have encountered patients who had recieved various types of cardiac valve replacements. Follow on anti-coagulant therapy varied from anti-coagulants for the rest of their life to just ASA therapy for a few weeks. Which depended on what type and material of valve replacement was used. I was unsure where a PFO patch would fall in this spectrum.

While the TEE would be primary I didn't know if some other test would as a side benefit provide diagnostic information as sometimes happens in other testing.