A Nasty incident

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Sebastian, you might want to click around and do some research on PFO...it affects a certain percentage of the human population, but it isn't hereditary. It isn't developed in adulthood, it is how you are formed (or not) at birth.

Now here is a bit of research that I don't expect has been done....is the instance of PFO higher among those of us who were "preemies?"
 
Sebastian once bubbled...
so how do you get a PFO?
We all have had one, because it is needed before we are born. It is just that in at least 30% of the population closure is incomplete after birth. This seldom produces any symtoms whatsover, or natural selection would have eliminated it but is thought to be associated with a four-fold increase in the incidence of strokes in later adult life. Indeed many athletes must have one and not know it, as I did, and I was very fit (more so when I was younger).

The only thing that happens is that a very small proportion of the oxygenated blood in the left atrium finds its way to the right atrium so it goes aroung the lungs again (a left to right shunt).

More detail (an edited copy of an earlier post of mine).

Any arterial bubble can cause the severest type II DCI but bubbles first form in the veins and tissues, not in the arteries, as the absolute pressure in the arteries is much greater.

It is now believed that small bubbles always form in the veins during the ascent from any dive. Thankfully blood from the veins must first pass through the right side of the heart and then to lungs, where even the smallest in size are mopped up by lodging in the pulmonary capillaries where they do little damage.

Although bubbles can form in the tissues, causing localised damage (usually type I DCI) a more serious form of DCI is when bubbles find their way into the body's arterial circulation and lodge (embolise) in the small vessels of the vital organs such as brain, spinal cord and even the heart (the coronary circulation) where they cause local damge. Obstruction of the arterial supply to these organs stops the supply of life-giving oxygen, causing the damage frequently recognised as DCI type II.

In an adult there are two circulations left and right, which act in series. The left ventricle pumps blood around the body at high pressure, which is then returned to the right side of the heart where the right ventricle pumps exactly the same amount of blood to the lungs, but at a significantly lower pressure.

A PFO is a persistent, usually flap-like opening between the two atria of the heart. It is essential to intrauterine life where the lungs cannot function and very little blood passes through the pulmonary vessels. In the foetus both sides of the heart act in parallel. This means that the right ventricle receives some of the venous return from the body and most the blood that is normally pumped through the lungs by the right ventricle finds its way directly to the aorta (a part of the left side of the circulation),via the ductus arteriosus; another intentional right to left shunt.

After birth the lungs expand, the pulmonary vessels open up and the pulmonary circulation becomes established. The increased left atrial blood flow and pressure results in functional closure of the foramen ovale simply because of this pressure change. In the majority, the flap valve is subsequently permanently sealed. However, closure is incomplete in up to 25-35% of adults in which case a small percentage of high pressure blood from the left atrium finds its way into the right atrium depending on the size of the defect; a left to right shunt.

By itself a left to right shunt is not problematic for divers, since as we know this blood goes to the lung filter. There are circumstances, however, when the shunt is reversed. This occurs when the right atrial pressure is greater than the left (following a transient increase in venous return). Examples include coughing and sneezing and the end phase of the Valsalva manoeuvre, when the pressure within the rib cage is temporarily increased and then released. This is also a feature of pulmonary barotrauma. Any bubbles present in the venous blood can find their way into the arterial circulation by the means this right to left shunt and cause an "unexpected" DCI, particularly the more serious type II.

Echocardiography can demonstrate the presence of a PFO, which can be detected in up to 20% of healthy adults which is now routinely excluded after any type II DCI hit.

At present imaging echocardiography is not useful for the screening of diver recruits. It is expensive, at over £600 a time, and it is not always accurate. However, when detected, a PFO can be closed by an umbrella device, which is inserted via a peripheral vein and thence into the heart.
 
Dr Paul, I doubt that 'bubbles' caused the problem. You may want to invest in a PET scan.
 
Welcome back! I am ashamed to admit that I didn't even know you were sick.

That settles it! I'm taking the rescue diver's coarse this summer, even though it is in the cold quarry (compared to Cozumel). Have been thinking of doing it anyway, but now I definitely will.

What percentage of O2 were you using, if I may ask, and was the lung injury due to drowning or pulmonary barotrauma?

ET
 
Dr Paul Thomas once bubbled...
Fresh water drowning;- all caused by osmosis.

Instead of air, low osmotic pressure fresh water finds its way into the alveoli. Since the osmotic pressure of water is infinitely less than that of the plasma there is a mass transfer of water from the alveoli into the pulmonary vascular bed. This, of course dilutes the arterial blood.

This subsequently results in mass transfer of fluid from the (diluted) plasma into all muscle and connective tissue cells and interstitium, resulting in swelling of these cell types; seen as oedema.

One of the affected cell types is the erythrocytes, which swell and burst due to the stretching of their cell walls to accomodate the greatly increased volume within the cells; haemolysis. This releases haemoglobin molecules into simple solution. Anaemia and asphyxia results . In addition these molecules clog the filter mechanism in the glomerulus of the kidneys; which are no longer able to function.


I had assumed that the acute renal failure (ATN) was due to hypotension secondary to drowning and prolonged apnea with failure of the circulartory system. Of course, hemoglobinurea could cause acute renal failure as well. Perhaps there might have been some myoglobinemia with myoglobinurea as well, which as well can cause acute renal failure.

To me, the main question is, "What caused your seizure?"

I don't know what % of O2 you were breathing -- I think you said you were breathing Nitrox? One thinks immediately of OxTox, but it sounds like you were at much less than MOD for your EAN%, right? Have they done an MRI of your head to look for focal lesions which could cause a seizure? How about an EEG? Have you had previous head trauma which could have caused a scar with subsequent seizures? Any history of epilepsy in the family?

Could your breathing gas have been contaminated?

You attributed your survival partially to the very cold water, but I thought that the advantage of drowning in cold water was that it usually generates hypothermia, which you may not have had because you were thermally protected by your dry suit.

Just trying to analyse,

ET:doctor:
 
DivingDoc once bubbled...
. . . renal failure (ATN) was due to gross haemolysis.

To me, the main question is, "What caused your seizure?"

I don't know what % of O2 you were breathing --

ET:doctor:
Hi DivingDoc,

I am not sure I "fiited" I believe my "shallow water blackout" was due to raised intracranial pressure due to expansion of those nasty bubbles (which may also have caused localised obstruction of blood flow). I was using Nitrox 32 at 22 M.

By the way, why does pescador think a PET scan would help?

Kind regards,

Paul
 

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