Do you know about Immersion Pulmonary Edema? You should...

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Claudia,

I really have no comment other then to say thank you for the interesting and informative article. I hope to see the study being done by Duke come out soon.
 
Claudia, I suspect that with the diffusion difficulties presented in pulmonary edema, an inspired ppO2 of 1.6 or even 2.0 would not translate into an arterial pO2 anywhere near that high. As I said, in all accounts I have read of significant cases of this illness, the patients have been cyanotic at the surface, which represents a major desaturation of hemoglobin.

It wasn't a recommendation, but it was a thought. I suspect that, if I felt I had IPE and I was terribly short of breath and facing a deco obligation, I'd switch to my hottest mix as soon as possible and see if it alleviated the symptoms at all. As you know, air hunger is usually CO2, and by the time you are short of breath from hypoxia, you are hypoxic indeed. Of course, the dyspnea of IPE may also be in part increased work of breathing with stiff, fluid-filled lungs, and in severe cases, there may be enough interference with gas transport to raise the CO2 as well.
 
In early 2011 my wife's best friend died from IPE on a dive I organised. Here is an article about what happened Michael McFadyen's Scuba Diving Web Site.

There are also some links to papers by Dr Carl Edmonds on this case and generally on IPE.
 
@clownfishsydney very sad story, condolences.

@mods, would it possibly be worth having a specific IPE sub-forum given that this condition seems to be more prevalent than previously thought? At the very least it might serve as a decent repository for similar type incidents and might be easier to trawl thru for information? Just a thought.

John
 
n;
Is your account written up anywhere? Anyhow glad you're back in the saddle and doing well.

John

Look in "Accidents and Incidents">"Near Misses and Lessons learned": My report is there. "Close Call"
 
Dr. Roussos, great writeup. Thank you for sharing.

There may be a difference between the IPE that occurs in triathletes/combat swimmers and the IPE that occurs in recreational divers. In over 50% of the recreational dive population, there is an identifiable comorbidity (e.g. hypertension) that could contribute to the occurrence of IPE. It can be very difficulty to differentially diagnose immersion pulmonary edema in the field. Anyone who is exhibiting signs or symptoms of pulmonary edema needs immediate medical attention.

There is some data we haven't yet published, but I would definitely agree with the statement that overhydration can be a contributory factor in people who are already susceptible to IPE. This is NOT repeat NOT an admonition to underhydrate during a dive series. Adequate hydration is beneficial. Chugging 2 liters of Gatorade before a dive when you're already adequately hydrated may not be ok.

Is IPE less likely with a drysuit? There is no immersion in water, nor a cold shock on entry. The pressure increase from immersion is still a factor. Physiologically, drysuit immersion seems quite different. Has anyone done a differential study of dry vs. wet diving?

No, being in a dry suit does not change the effects of immersion in water but certainly can alleviate some of the effects of temperature.

@Dr Moon, are there or have you any plans to publish your findings to date? Would make very interesting reading even if firms conclusions can't be made.

Thanks,
John

We recently completed a study that involved placing pulmonary artery catheters in individuals with previous incidents of IPE and measuring the effects of a medication on pulmonary artery pressure. Dr. Moon is in the process of writing it up; look for it within the next two or three months. We're also in the midst of studying the effects of overhydration. Additionally, we're looking at tricuspid valve regurgitation as a potential factor by performing immersed cardiac ultrasounds.

Best regards,
DDM
 
I have updated the write up on my web site (in a previous post) to include information from the coroner's inquest as well as an interpretation of the dive computer printout (with air consumption) from the fatal dive. The link is Michael McFadyen's Scuba Diving Web Site.
 
One small point that may be worth noting for anyone with an interest.

I was advised that IPE actually gets worse on ascent. I initially assumed this would be because of the reduced PPO2 but was advised that is was because fluid in the lungs getting redistributed by expanding gas - essentially making the gunk spread further in the lungs and exacerbating the symptoms.

If this is the case is there any merit in trying to have the slowest ascent possible or is it more important to get topside and on O2 ASAP?

Thanks,
John
 
One small point that may be worth noting for anyone with an interest.

I was advised that IPE actually gets worse on ascent. I initially assumed this would be because of the reduced PPO2 but was advised that is was because fluid in the lungs getting redistributed by expanding gas - essentially making the gunk spread further in the lungs and exacerbating the symptoms.

If this is the case is there any merit in trying to have the slowest ascent possible or is it more important to get topside and on O2 ASAP?

Thanks,
John

John,

I don't think there is any physiological basis for that. Expanding gas in your lungs is exhaled and doesn't get an opportunity to press against the alveoli. That is, unless you're holding your breath, which would set you up for bigger problems than IPE.

I think that the best course of action is to do is exactly what both you and Claudia did fantastically well, which is to get to the surface as soon as safely possible while being mindful of your your decompression obligation and any changes in your condition.

Best regards,
DDM
 
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