Pulmonary Oedema incident

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John, welcome back! I have just a couple of comments... One of the side effects of propranolol is emotional in nature. While I'm not saying this is related to your incident, it could be a problem. The drug can make one feel depressed or apathetic, two things that are not compatible with diving. Next is training. You and your buddies have obviously taken indepth training seriously. The more detailed to training the better prepared is the diver to handle situation. Many of the dive related incidents I read seem to have less than adequate training as a factor. As divers we wanted more and more people to experience the joy we get underwater, but God placed us on land for a reason. I feel that even basic OW certification may come to easily to some. The final point is honesty. I absolutely loves being underwater, and would be devastated if I couldn't dive. John, just between you and me, I think sometimes I ignore things about my body because I'm afraid if I address them I may not be able to dive. I know from talking to other guys I am not alone. The cosmic issue I deal with is, if I have a health problem at depth, and hurt myself that is my choice. If I have an issue at depth and endanger my buddy, that's something quite different.
I have resolved the issue in my mind(much to the relief of any potential dive buddies). It would be interesting to hear from others who have opinions about this.
Thanks
 
My apologies if this has been addressed elsewhere in this thread as I did not read every single post. However, after reading the OP's account, this strikes me as as a highly probable case of Negative Pressure Pulmonary Edema, as opposed to Immersion Pulmonary Edema or any other variant of fluid collection in the lungs. As an anesthesiologist I'm aware of a few instances where this has occurred in the postoperative setting. In contrast to many other etiologies of pulmonary edema, NPPE has a very specific casuse. In fact, it most frequently been described in relatively young healthy individuals who are able to generate high negative intrapleural pressures against some form of airway obstruction, such as laryngospasm. The muscles of the chest wall attempt to take a large breath, producing large negative inspiratory pressures. When air cannot be drawn into the lungs, the difference between intrapleural and interstitial pressures favors rapid accumulation of fluid in the alveoli. The pathophysiology has not been fully worked out but some form of endothelial membrane injury (acute lung injury) may contribute to the phenomenon by permitting fluid exchange into the airways. The diver's description of having to suck hard against significant airway resistance, followed fairly rapidly by worsening hypoxia, make a strong case for negative pressure pulmonary edema. This also fits a pattern of relatively rapid resolution of symptoms as return of normal starling/circulatory forces will lead to clearing of the alveolar fluid. I'm glad that things worked out OK and the assistance you received getting to the boat and immediate O2 once on board certainly were critical to a favorable outcome. Good lessons for us all. Thanks for sharing your close call.

From Inthedrink's post:

"We then dropped down to 40m and did some simulated H and boom drills. I did have a slightly hard time the couple of times I’d tried to just use the ADV on descent, having to take some pretty serious sucks to get enough gas. I went back to manual add after this. "
 
My apologies if this has been addressed elsewhere in this thread as I did not read every single post. However, after reading the OP's account, this strikes me as as a highly probable case of Negative Pressure Pulmonary Edema, as opposed to Immersion Pulmonary Edema or any other variant of fluid collection in the lungs. As an anesthesiologist I'm aware of a few instances where this has occurred in the postoperative setting. In contrast to many other etiologies of pulmonary edema, NPPE has a very specific casuse. In fact, it most frequently been described in relatively young healthy individuals who are able to generate high negative intrapleural pressures against some form of airway obstruction, such as laryngospasm. The muscles of the chest wall attempt to take a large breath, producing large negative inspiratory pressures. When air cannot be drawn into the lungs, the difference between intrapleural and interstitial pressures favors rapid accumulation of fluid in the alveoli. The pathophysiology has not been fully worked out but some form of endothelial membrane injury (acute lung injury) may contribute to the phenomenon by permitting fluid exchange into the airways. The diver's description of having to suck hard against significant airway resistance, followed fairly rapidly by worsening hypoxia, make a strong case for negative pressure pulmonary edema. This also fits a pattern of relatively rapid resolution of symptoms as return of normal starling/circulatory forces will lead to clearing of the alveolar fluid. I'm glad that things worked out OK and the assistance you received getting to the boat and immediate O2 once on board certainly were critical to a favorable outcome. Good lessons for us all. Thanks for sharing your close call.

From Inthedrink's post:

"We then dropped down to 40m and did some simulated H and boom drills. I did have a slightly hard time the couple of times I’d tried to just use the ADV on descent, having to take some pretty serious sucks to get enough gas. I went back to manual add after this. "

My personal suspicion, backed up with no evidence :D is that negative pressure / hard sucking may indeed have contributed to the episode. A few months back I was a bit too raw mentally to really say that as I was worried it might be construed as a criticism of the rebreather, especially as there is no evidence that this is what caused the issue. However, now that I'm a little more clear headed about the incident my feeling is that my operation of the CCR may have been a contributory factor. The CCR I was using has back mounted counter lungs, fairly small counter lungs (certainly in comparison to the other rebreather I trained on initially) and has a somewhat understated ADV. The recommended SOP is to use the manual add button on the back rather than use the ADV. I think because after the initial drills I was tired and task loaded I disregarded the SOP and just relied on the ADV to inject diluent. As we were descending reasonably quickly at the time, this really wasn't a great decision (which I recognised and after a couple of hard sucks and reverted back to manual add). My episode started a 3 or 4 minutes after this hard sucking, but this could be coincidence.

None of this is to negate the other factors that may well have played a role in this episode, namely several medications that have been associated in one way or another as potential contributors to reduction in heart output/other things that could contribute to pulmonary edema. Various commentators have suggested that the entire combination of factors may have created something of a 'perfect storm'.

Which is why I have worked hard since the event to remove pretty much all of these factors (more exercise, reduced alcohol, improved diet, no medications of any description, no CCR) under the presumption that this should reduce the risk significantly. Other commentators (DAN Asia) have equally suggested that I am deceiving myself and that the risks remain pretty much unchanged as they still don't really understand why SDPE occurs.

In any event, I'm just glad to be back diving and will be taking it nice and easy for the time being. I have a quick question for you - I have been told that in a post operative setting that Lasix is used in the event of pulmonary edema (in addition to O2). Is this something that you think make sense to have in my armory (IV) for my buddies/rescuers to be able to use should a similar event recur?

TIA,
John
 
The theory behind Lasix administration is two-fold. One is that the edema is due to total body fluid overload (which it rarely is) and the other is that Lasix causes a degree of dilation of the veins, thus reducing blood return to the heart and therefore pooling in the pulmonary vessels. This is difficult to prove, and a number of recent studies have shown poorer survival for cardiogenic pulmonary edema patients when Lasix is used. Since the diagnosis of what is causing breathing problems in a diver can be difficult, even for professionals, I certainly would not advise someone to carry this drug and encourage one's lay diving companions to administer it.

Positive pressure oxygen is probably more useful, but again, doing positive pressure ventilation with a mask is something rarely done well without training. However, if I had had an episode of IPE and decided to dive again, I would certainly ensure that oxygen was available anywhere I was diving, shore or boat.
 
Thanks Lynne,

I have become rather more particular about ensuring O2 is on any boat I'm on. Thanks for the heads up on the Lasix. What you say makes sense. I'll speak to my dive doctor, obviously, and get his take. We're not clear on whether my episode was cardiogenic in nature or not (all heart tests came back fine although what this proves I'm not sure. I managed the final level of the Bruce protocol still walking (fast) and with no bother. All valve function and output were normal from what the reports said).

Thanks again. Silly addendum but worth sharing maybe. Before my incident I used to get myself to sleep every night imagining kitting up. I never ever managed to kit up fully before I fell asleep. Kinda like scuba sheep counting. Anyhow, after the accident I just couldn't bear to think about diving much less try to get myself to sleep thinking about it. Initially all I dreamt about was coffins and waking up in suitcases and other sub-optimal dreams.

Since my trip to Key Largo, I've been waking up kitting up again. Waking up think about why my left foot is slightly non horizontal in the load part of my kick. Damn it feels good to be back. Taking a few people diving on Sunday to see whether I can help them improve their skills. Can't wait.

J

---------- Post added April 24th, 2012 at 10:16 PM ----------

A newer medical paper publish last month is on my web site http://www.michaelmcfadyenscuba.info/downloads/SDPE%20Fatalities%20DHM%202012.pdf. A report about a dive where our close friend died of immersion (or scuba divers) pulmonary oedema is on my web site at Michael McFadyen's Scuba Diving Web Site. Carol is mentioned in the medical paper.

Sobering. To say the least.

---------- Post added April 24th, 2012 at 11:28 PM ----------

A newer medical paper publish last month is on my web site http://www.michaelmcfadyenscuba.info/downloads/SDPE%20Fatalities%20DHM%202012.pdf. A report about a dive where our close friend died of immersion (or scuba divers) pulmonary oedema is on my web site at Michael McFadyen's Scuba Diving Web Site. Carol is mentioned in the medical paper.

Hi Michael,

I've read a resonable number of the reports and whilst I'm no statistician I haven't been able to get a handle on how the recurrence rate has been calculated. Is there any info on this as obviously I'd consider myself an interested party? recurrence within 1 yr? 5 yrs? 100 dives? Was time not considered? What about the sample that didn't have recurrence? Did they have the same number of additional dives to the divers where it did recur? What was the percentage fatality rate? I'm probably asking stupid questions but I've found the blanket 30%+ recurrence rate in the absence of context somewhat hard to understand.

Thanks,
John
 
Thanks for the opportunity to read and learn from your experience! I am so glad you are back in the water and hope you have many more safe years of diving. Some thread just deserve to be reactivated!
 
John, sorry but I do not have any answers to your questions. Dr Edmonds is in Europe on a holiday at the moment so I cannot ask him. If you remind me via my email (on my web site) in a month I will ask him.
 
I recall reading that using low dose Nifedipine and Viagra have been considered for use in SIPE patients when they return to in water activities. I have not been able to locate any literature looking at this (SIPE specifically, although I found studies investigating Viagra use for other types of pulmonary edema). Anyone have any info ?
 
Sorry for the huge delay in the IPE article. A new Editor for the newsletter wasn't found until recently, but the Fall 2012 newsletter with IPE, CO and other articles is finally up on the OUC website at:
http://www.underwatercouncil.com/dow...newsletter.pdf

Hope you find it informative,

Ayisha
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