A Question for You Navy Docs

This forum made possible through the generous support of SDN members, donors, and sponsors. Thank you.

island doc

Senior Member
10+ Year Member
5+ Year Member
15+ Year Member
Joined
Jul 24, 2005
Messages
494
Reaction score
4
I have a serious question for any of you Navy physicians, question is probably best suited for a dive MD.

I recently read a newspaper article about a cave diver who died after mistakenly taking only one single breath of 100% oxygen at a depth of 120 feet during ascent from a deep cave dive.

His companions reported that he seized and died instantly.

Can any of you please explain the pathophysiology behind this? I am quite curious to know. Even though I am surrounded by water, I have no dive training or experience. Thanks.
 
Oxygen toxicity my friend.

100% oxygen at 4 atm.....That is a partial pressure of Oxygen of greater than 3000 mmHg....

Seizure is a known complication of oxygen toxicity in hyperbaric environments....although it shouldn't happen right a way.
 
I have a serious question for any of you Navy physicians, question is probably best suited for a dive MD.

I recently read a newspaper article about a cave diver who died after mistakenly taking only one single breath of 100% oxygen at a depth of 120 feet during ascent from a deep cave dive.

His companions reported that he seized and died instantly.

Can any of you please explain the pathophysiology behind this? I am quite curious to know. Even though I am surrounded by water, I have no dive training or experience. Thanks.


My question is what was he doing with a 100% oxygen supply anyway? The only explanation is that he was not on open-circuit but on a re-breather. For cave diving and videography underwater, rebreather gear is sometimes used to keep the water clear of SCUBA exhaust gas bubbles. But that kind of highly-specialized dive gear is supposed to keep the gas mix precisely regulated so as to avoid all types of hyperbaric toxicities.

My guess: he got bent and took a CNS hit.
 
My question is what was he doing with a 100% oxygen supply anyway? The only explanation is that he was not on open-circuit but on a re-breather. For cave diving and videography underwater, rebreather gear is sometimes used to keep the water clear of SCUBA exhaust gas bubbles. But that kind of highly-specialized dive gear is supposed to keep the gas mix precisely regulated so as to avoid all types of hyperbaric toxicities.

My guess: he got bent and took a CNS hit.

The caves they were diving are very deep, at 300 and 360'. I seem to recall reading that they were using the pure oxygen to aid in decompression.

By the way, these paricular caves called Diepolder II and III are the deepest in the US, and are located on a Boy Scout Camp north of Tampa near Spring Hill, Florida. They are the holy grail of cave divers in the US.

www.floridacaves.com/diepolderfatality.txt
 
This unfortunate Italian was doing a mixed gas deep dive using a scuba rig. He actually donned several tanks with Nitrox (or Helox) and one with 100% oxygen to be used at the last decompression stop. Breathing 100% Oxygen while decompressing is beneficial in two ways: 1) increases nitrogen off-gassing thus reducing the possibility of getting "bent" (DCS) and 2) decreases decompression time. But 100% O2 below 20 FSW (feet of sea water) is toxic and will likely cause an O2-hit (O2 toxicity). The deeper the diver, the more likely and severe the O2 hit will be. In the case of this diver, he took a breath form the wrong regulator (100% O2 vs. Nitrox) at 190 FSW producing a severe O2 toxicity reaction (seizure) rendering the diver unconscious. At that moment he was a great candidate for BLS protocols which are very hard to deliver at 190 FSW. Additionally, his companion cannot bring the injured diver staright to the surface since he also requires several decompression stops. In conclusion, this fatal mistake can be attributed to O2 toxicity after breathing from the wrong tank at 190 FSW. Then he drowned or had an AGE. Hope this helps…

DiveMD
 
Thanks for the clarifications. I am considering taking up open water diving. I don't know about caves though...

I should ask our friendly caveman what it's like being in his home when it's flooded...
 
Oxygen toxicity my friend.

100% oxygen at 4 atm.....That is a partial pressure of Oxygen of greater than 3000 mmHg....

Seizure is a known complication of oxygen toxicity in hyperbaric environments....although it shouldn't happen right a way.

Ditto. I would also consider oxygen atelectasis.
 
Ditto. I would also consider oxygen atelectasis.

I disagree with the Pulmonary O2 tox diagnosis. This is a classic CNS hit secondary to high O2 levels. In order to develop pulmonary O2 toxicity a longer exposure at high PO2 levels is required (O2 breaks down surfactant causing atelectasis). But in this case, the CNS symptoms showed up immediately after breathing form the wrong regulator. Such a short period of time is not sufficient to actually develop a fatal atelectasis. Plus, he had SEIZURES…….CNS O2 TOXICITY!!!
 
Thanks for the clarifications. I am considering taking up open water diving. I don't know about caves though...
Leave caves alone for now. Regular old scuba is incredibly safe. Wait until you have a minimum of 100-200 dives before doing any cave diving, which at one point accounted for something like 1/3 of all dive fatalities even though it's less than 1% of all diving.
 
That's a myth.

Don't mean to butt into a Navy thread, but...

militarymd is correct. In 15 years of doing anesthesia, I have never seen this supposed clinical entity in a living, breathing or non-breathing, human patient, vs. some lab rat somewhere in Eastern Europe.

I *have*, however, witnessed more than one near death experience when CRNAs force their SRNAs (excuse me, NARs) to wake up a sick patient on less than 50% FiO2 in order to avoid this dreaded, mythical complication. I have been forced, on rare occasion, to take it upon myself to turn the air down to 0 l/m and the O2 up to 10 l/m on emergence, over the cacophonous, braying objections of those dolts with way too Little Learning combined with way Too Much Rank.

A little learning is a dangerous thing;
Drink deep, or taste not the Pierian spring:
There shallow draughts intoxicate the brain,
And drinking largely sobers us again.

Alexander Pope, Essay on Criticism, Part II, line 15

--
R
http://www.medicalcorpse.com
Yes, I realize that this forum is not AP English, nor AP Latin. Deal.
 
I *have*, however, witnessed more than one near death experience when CRNAs force their SRNAs (excuse me, NARs) to wake up a sick patient on less than 50% FiO2 in order to avoid this dreaded, mythical complication. I have been forced, on rare occasion, to take it upon myself to turn the air down to 0 l/m and the O2 up to 10 l/m on emergence, over the cacophonous, braying objections of those dolts with way too Little Learning combined with way Too Much Rank.

It's like EMS and a lot of nursing personnel and the "O2 will make a COPD'er stop breathing!" rumor. I can't tell you how often I've had to explain the idea of hypoxic drive....."Besides, if you do, by some bizarre chance alignment of the planets, stars and the whims of whatever invisible man in the sky you choose to worship, knock out their drive to breathe, it just makes them easier to intubate! Think of it as poor man's RSI."

I actually had a newbie EMT rip a simple face mask off of a COPD'er
"You're going to kill him! You can't give him that much O2"
"No, if you don't give me that back and apologize to Mr ********* for scaring him even more than he already was, I think you have more to fear from me than he does." *points at captain's bars on my collar*
"So? You outrank me....that doesn't mean you know what you're doing!"
"Yes, but which one of us is a respiratory therapist you nitwit? And which one of us will have our EMS certification once Dr. ******** (our medical director) finds out about this?"
*grabs SFM and puts it back on the patient*
The patient turns and looks at him and goes "You...son....are.....a dumb.....sumbitch." :meanie:
 
It's like EMS and a lot of nursing personnel and the "O2 will make a COPD'er stop breathing!" rumor. I can't tell you how often I've had to explain the idea of hypoxic drive....."

This thread made me remember an episode I am including in my book, but which I had forgotten to add to my website:

"Is that a Stork or an Angel I See?"

start off with the lead pic on my index page, then follow the link to the true story:

http://www.medicalcorpse.com/

--
R
Dum spiro, spero.
 
The REAL Air Force Core Values:
1. Self-promotion first
2. Half-assedness in all that we do
3. Service only thy self (not like that, I'm sure you can find a junior officer to do that for you....it makes a good OPR bullet :meanie: )
 
That's a myth.

I don't know about atelectasis, but we do see pulmonary O2 tox during hyperbaric chamber treatments. Injured divers with pulmonary symptoms usually report a burning sensation while breathing 100% O2 under pressure. Once you switch to regular AIR the burning sensation is gone. Plus, 100% O2 at 1 atm will behave diffrently form 100% O2 at >3 atm.
 
I don't know about atelectasis, but we do see pulmonary O2 tox during hyperbaric chamber treatments. Injured divers with pulmonary symptoms usually report a burning sensation while breathing 100% O2 under pressure. Once you switch to regular AIR the burning sensation is gone. Plus, 100% O2 at 1 atm will behave diffrently form 100% O2 at >3 atm.

Atelectasis (alveolar collapse) is not the same as pulmonary edema (alveolar filling/flooding).
 
You might want to read up on that a little more .....it's pulmonary edema

New England Journal circa 1983

I understand the main mechanism for hypoxia is pulmonary edema. Vessel leakiness is the sine qua non of any inflammatory response. But my point is that atelectasis is also present due to surfactant break down . It is not the principal cause of improper oxygenation, but is also there. One 1983 abstract is not sufficient to prove me wrong.

Search for this one: New Horiz. 1993 Nov;1(4):504-11
 
Alveolar collapse is the single most common entity to cause infiltrates and other radiographic findings on cxr or Chest CT.....it accompanies a variety of lung injury and/or lung parenchymal change...including alveolar filling....

However, alveolar collapse is not caused by oxygen absorption...like I said, that is a myth.
 
When did I use the term "oxygen absorption"? My only point is that atelectasis is one of the clinical findings during significant pulmonary O2 toxicity. Isn't that true?
 
When did I use the term "oxygen absorption"? My only point is that atelectasis is one of the clinical findings during significant pulmonary O2 toxicity. Isn't that true?
yes
 
Top