apitkin

There are obviously no randomised controlled clinical trials, the gold standard of evidence in medicine. So what we are left with is some theory and some less good evidence.

The theory that links DCI risk to the presence of a PFO is based on the simple idea that venous gas bubbles pass through the PFO to the arterial circulation, where they cause clinical symptoms by being carried to the affected organs, principally the central nervous system. So it makes sense that closing the PFO with a device should reduce the risk of DCI.

However, it is clear that the disease entities grouped together as DCI are not all caused by embolisation (travel in the bloodstream) of gas bubbles. It does not explain why, for example, the spinal cord is often so badly affected in severe DCI as this is way out of proportion to its blood supply. (It is probable that gas bubbles form in situ in the spinal cord due to its content of lipid-rich myelin.)

So it may be that closure of a PFO only reduces the likelihood of certain types of DCI.

But there's more. In animal experiments it has been observed that gas bubbles form on any foreign material within the heart (such as central venous catheters) when those animals are subjected to severe decompression stress. It could be that a closure device acts as a focus for bubble formation within the heart, thereby actually increasing the risk of DCI.

Now, I have no evidence that this actually happens, but I am pointing it out as a possible example of the law of unintended consequences which acts so often in medicine.

Many eminent diving doctors are not convinced of the usefulness in terms of overall balance of benefit and risk of having a PFO (as opposed to a significant ASD) closed, and I share their scepticism. You will, I dare say, hear a different point of view from the cardiologists, but most of them know very little about the pathophysiology of diving disease.

Andy