Fatality off Bald Head Island - NC

[Jax]

My concern in pushing this point is that we may be missing an opportunity to help someone who has IPE. The first aid to IPE is not JUST CPR - it is forcing oxygen into the flooded lungs. (See DeniseGG's thread / description and the DAN article written by an IPE victim.)

Forcing air means use of a continuous positive airway pressure (CPAP) machine, or by a rescue breather inhaling O2 and forcing it into the victim's lungs. How many people know to do that??? It certainly isn't trained in rescue diving.

Although rare in people exercising on land, pulmonary edema is more routinely reported in individuals participating in swimming or other immersion-related sports.10 Adir and coworkers describe a series of 70 teen athletes who, over a 3-year period, developed SIPE.10 All cases occurred in trainees who were swimming semi-reclined in warm seawater and wearing fins. Similarly, Koehle and associates reviewed 60 published cases of immersion-induced pulmonary edema in 56 individuals. Only 9 cases were associated with endurance swimming. The rest were associated with scuba diving and breath-hold diving.¹¹ Three cases of right-sided pulmonary edema were described in men who swam right side down during US Navy SEAL training manoeuvres.¹²

- A swimmer's wheeze - answer | Canadian Journal of Emergency Medicine

 

[Jax]

Hope some are learning from this stuff.

from Swimming-induced pulmonary edema: clinical presentatio... [Chest. 2004] - PubMed - NCBI

BACKGROUND:

Acute pulmonary edema has been noted in swimmers and divers, and has been termed swimming-induced pulmonary edema (SIPE). The mechanisms and consequences of SIPE are unknown, and there are currently no series of carefully evaluated patients with this condition. Herein we report the clinical presentation, incidence of recurrence, findings on physical examination, chest radiography, and oxygen saturation in 70 trainees with a diagnosis of SIPE. We also report the results of forced spirometry in a subgroup of 37 swimmers.
METHODS:

SIPE was diagnosed when severe shortness of breath and cough were reported during or after swimming, and were associated with evidence of pulmonary edema. During the years from 1998 to 2001, 70 cases of SIPE were documented in young healthy male subjects participating in a fitness-training program. Physical examination and pulse oximetry were performed immediately. Chest radiographs were obtained in all cases 12 to 18 h following onset of symptoms. In 37 swimmers, spirometry was performed at the time of chest radiography and again after 7 days.
RESULTS:

All subjects complained of severe shortness of breath. Sixty-seven of the 70 subjects (95.7%) had a prominent cough; in 63 subjects (90%), there was significant sputum production. Hemoptysis was observed in 39 subjects (55.7%). Mean arterial oxygen saturation after swimming was 88.4 +/- 6.6% breathing air, compared with 98 +/- 1.7% breathing air at rest before the start of the swimming trial (mean +/- SD) [p < 0.001]. Chest radiographs obtained 12 to 18 h after swimming were normal in all cases. Sixteen trainees (22.9%) had a recurrence of SIPE. Spirometry demonstrated restrictive lung function, which persisted for a week.
CONCLUSIONS:

In our trainee population, SIPE is a not uncommon, often recurrent phenomenon that significantly influences performance. It is not clear what predisposes to its occurrence or recurrence and what, if any, are its long-term effects.

 

[Jax]

One point on all these articles -- they are about swimmers.

Think about it -- divers may not surface in time to survive. What will the coroner find? AGE and / or drowning.

Maybe a cardiac. Is the cardiac the cause? Or did IPE cause a cardiac?

We DON'T KNOW enough about this, but knowing that when a bloody froth shows up, in a swimming / diving victim, a CPAC or other forced O2 should be used is IMPORTANT.

By the way, this isn't my opinion -- the Baywatch of Los Angeles now carry CPAPs in their immediate response gear, for just this reason.

(Source - Baywatch demo and discussion during USC's ERD class.)

 

[fpsndiver]

Thanks for the details. I am not qualified for much here, but anyone with a Nitrox card would have to wonder why anyone else would suspect OxTox - much less use words like "obviously."

Jax's suspicions on IPE seem more likely, one of those scarey wild cards in diving that we can't anticipated - more under the Caca Happens" umbrella. Certainly looks like a conservative dive planned and executed by experienced divers with no reason to expect problems.

Quite frankly, I wonder why anyone with a nitrox card would eliminate OxTox? You have a oxygen analyzer advertised in your tag line Don, what is the purpose of measuring the percentage of oxygen in one's bottom mix? What is the oxygen clock, and the dangers of elevated partial pressures of O2? The primary focus and drive behind the necessitation of NITROX classes was to educate those whom used it of the hazards associated with its use, primarily CNS Toxicity. CNS Toxicity is not completely and thoroughly understood. Several factors increase susceptibility: immersion, CO2 intake, workload while diving, etc. Any or all of these factors may or may not have been present during this dive that combined with other factors could have increased the divers personal susceptibility to CNS Toxicity. To completely discount CNS Toxicity is to ignore your training. CNS Toxicity is the main reason you are required to "certify" to use Enriched Air Nitrox.

I'll also await the report, I am reading on IPE, and maybe that is another possibility, but I think to dismiss a CNS Toxicity event is premature. I still don't understand what is so personal about CNS? As stated by a previous poster, CNS susceptibility is a massive unknown with multiple variables. When nitrogen tables were in their infancy, some of those scientist thought that stuff was gospel too, and much of it has been disproven or modified. CNS limits are in their infancy, and while commercial divers have developed their own systems, Technical Divers have to operate in a completely different environment, completing their decompression while still immersed. I don't think it is quite as simple as you seem to imply Don.

 

[DandyDon]

Quite frankly, I wonder why anyone with a nitrox card would eliminate OxTox? You have a oxygen analyzer advertised in your tag line Don....

In my Signature area? Nope, I don't.

Yes, OxTox could be a possibility. Very unlikely from the data stated today, but doubtful IMO, and certainly not "obviously" as claimed by two in this thread.

On the other hand, I guess we have discussed all of the possibilities here, as well as how to avoid them if possible. IPE seems like an unavoidable wild card risk, but research continues. Maybe DAN will have more for us on that someday soon.

 

[ahava]

One point on all these articles -- they are about swimmers.

Think about it -- divers may not surface in time to survive. What will the coroner find? AGE and / or drowning.

Maybe a cardiac. Is the cardiac the cause? Or did IPE cause a cardiac?

We DON'T KNOW enough about this, but knowing that when a bloody froth shows up, in a swimming / diving victim, a CPAC or other forced O2 should be used is IMPORTANT.

By the way, this isn't my opinion -- the Baywatch of Los Angeles now carry CPAPs in their immediate response gear, for just this reason.

(Source - Baywatch demo and discussion during USC's ERD class.)

Like you said they are all swimmers. But the fact that they are, does not help the case for IPE. One critical ingredient is missing Higher then normal ppo2. How does this effect divers different then swimmers ? I dont know. So its hard to compare. Because you stated someone else who purged their 2nd stage the same way, could be revelant but also could just be a coincidence. Nothing can really be counted out, some are just more likely then others.

 

[Jax]

I'll also await the report, I am reading on IPE, and maybe that is another possibility, but I think to dismiss a CNS Toxicity event is premature. I still don't understand what is so personal about CNS? As stated by a previous poster, CNS susceptibility is a massive unknown with multiple variables. When nitrogen tables were in their infancy, some of those scientist thought that stuff was gospel too, and much of it has been disproven or modified. CNS limits are in their infancy, and while commercial divers have developed their own systems, Technical Divers have to operate in a completely different environment, completing their decompression while still immersed. I don't think it is quite as simple as you seem to imply Don.

I'm believing the other divers that the ppO2 did not exceed 1.4; in this case, the oxtox is a long shot. IMO. Such that it is.

 

[fpsndiver]

1.4 for how long? Was any CO2 contamination present in the tanks, what was the WOB on the regs? There are still a lot of unknowns that are against elimination of CNS, even if their mix was within limits. If they got a fill from a station that hadn't cleaned their filters, there is a possibility of CO2 contamination in the gas mix.....that CO2 could change your equation drastically. If aHeavyD and his partner got fills at the same location, aHeavyD's tanks should have been analyzed for CO2/CO and the usual suspects...He, N, and O. Teeth diving can be somewhat strenuous, depending on how much you dig, and this too could put CO2 into the equation. CO2 is a game changer with CNS Toxicity. This is why many rebreather divers dial their loops back to 1.0 or 1.2, as I've previously said. The risk of CO2 in their loops increases their susceptibility to CNS Toxicity. Open Circuit Divers have it a little safer, if the fills are from a reputable source, but there is still some risk of elevated CO2 levels from the diver. There are still a great deal of unknowns. They say they were at or below 1.4, then fine, assume they were. Does that absolutely eliminate CNS Toxicity? I say ABSOLUTELY NOT, especially with the symptoms described. If the autopsy shows no cardiac involvement, and just AGE....that evidence points very specifically at CNS.

and @Don, so it was a CO analyzer...my bad. I just read Analox. so....what I have to say here might make some sense to you as well. If you read the link I posted about CNS Toxicity, you can read what medical professionals have to say about other factors besides the rules that seemed to increase susceptibility...including some OTC medications that divers commonly use.

 

[Jax]

Sure there is a lot of unknowns, but the big problem with any sort of CNS tox is that the body metabolizes it.

Everything I have read about OxTox says convulsions, not someone purging a reg into their mouth. He was concentrating on getting air into his lungs all the way to the end. And how does a doctor decide it is AGE over IPE?

 

[fpsndiver]

Not all seizures are convulsive. OxTox seizures vary from person to person, and some are described as convusive seizures while others are described as catatonic stares and rigidity... My former girlfriend was epileptic, and when she seized it was a staring seizure, then she would be lethargic for several hours following the seizures, it was very scary. I don't know how a doctor differentiates between AGE and IPE. I have attended several autopsies, and I do know that ME's are pretty good at dissecting murders, heart attacks, liver disease, cancer, drowning, and smoke inhalation deaths...but as far as diagnosing diving injuries? Outside of their normal realm. That is what leaves many divers confused about some of their conclusions. The cause of death is always the same, drowning and AGE. That doesn't neccesarily mean that is the culprit that began the chain of events, merely the physiologically observable result.