HBO as precaution?

[perche]

Hi,

My questions are based on this story:

A dive was planned to reach a mark at 57m. Temperature in fresh water is 4-6C at 40m. Visisibility is 20cm between 0-20m, better under 30-40m (but everything is black…).

Diver 1 : CMAS level 4 (prep instructor)
Gear : 15l air, 2 regulators, « normal » stabilising jacket, dry suit.

Diver 2 : CMAS level 3 / nitrox 1 + 2 / dec tec (NAUI) /
Gear : 2X10l with manifold + one stage botte 6l filled up with 50%, unfortunately less 100b due to a bad manip before diving (Murphy’s law). BP + wing (classic DR).
Two regulators : a Legend with pressure gauge, direct system, and « octopus ». an Apeks 200 (baught the evening before the dive) with long hose as main, transmitter to computer and dry suit. He has wo computers : Vytec for deco and Aladin air z with transmitter because it’s an excellent alternative to the traditional wrist computer and analogue pressure gauge ( !!!! – dixit Uwatec ) .


At 50m Aladin’s diver2 (cmas 3) beeps : alarm rbt! Shortly after this alarm diver 2 starts to have difficult breathing. Aladin displays tank pressure as two « -- « ! diver2 shakes his lights to draw attention. But diver 1 was too far from diver 2 and didn’t see the signs. Diver 2 starts to ascent but becomes short of breath. He tries to see where was his buddy, but failed. He was too tired to act properly and gets some rest on a platform at 55m. After one minute diver 2 starts the ascent and at 35m tooks the stage botte. Diver2 surfaces. Aladin displays « SOS » and Vytec « err ». Last omited stop by diver 2 was at 6m 17min. dive time : 20 min. Diver 2 swims to a boat beside the coast, explains the situation and asks for an air bottle. The Intervall surface was 9min (The first botte given was empty – Murphy’s law). He stays 30min at 3m50 depth. Only one computer works: vytec in mode gauge.


Diver 1 (pre-instructor) says : I see the difficuties of my buddy and try to help him to ascent. Unfortunately I failed because his finger was stuck on the inflator. Then I saw my buddy lying in the bottom of the lake and his eyes was big open. Because I have only 100 bar in my bottle I surface. Hopfully I reachs a firefighter patrol. I got an O2 bottle and begins an in-water recompression to 9m depth surrounded by two people.

Why diver 2 ran out of air: It turns out the manifold between the double tank was closed (open by somebody and then before diving « re-open » by diver2) – a fact

Why the two divers didn’t react properly : probably due to narcosis – an opinion

Please, notice this thread is not an accident/incident analysis. The facts speaks for themselves. Please No "blamestorming.". Please, avoid to blame one of the diver and don’t. No trolling.

In summary we could say the two divers did a fast ascent and at least one diver omitted deco.

Fast ascent rate increase nuclei to grow to a sufficient volume to reach a point where DCS could develop. Perhaps omitted deco also…

There are also some possible « cérébral silent infarcts » or UFO in white matter that we didn’t talk too much among the divers….

So that these questions arise :

1) Are there some scientific works that substanciate and quantify the risk of silent infarcts or DCS in case of fast ascent and omitted stops?

2) In the situation described above is HBO tt necessary as a precaution and what is the policy in US?


Best regards

 

[perche]

In addition could we have any comments about the "in-water recompression" performed by the two divers.

thanks

regards

 

[perche]

Mistake!

Instead of

* Last omited stop by diver 2 was at 6m 17min" ,

please read

" At the end of the dive Aladin's diver2 displays: SOS, max depth 55, last stop (omitted) 15m 3', dive time 20' "


sorry

 

[Dr Deco]

Hello perche:

MRI Hyperintensities

To my knowledge, these bright areas [“T2-weighted hyperintensities” or “abnormal cerebral hyperintensities”] have not been shown to correlate with diving and DCS, in particular. (I believe that is what you mean by UFOs.) I have included recent references below that relate an increase in the number of bright areas with the presence of a PFO.

Another reference relates number of bright spots with DCS in goats.

These papers do not report on fast ascent rates or DCS and the MRI findings. Fast ascent rates are associated with more Doppler-detectable bubbles and an increased risk of DCS.

Decompression

It is my understanding (and my personal belief) that divers should not re-enter the water for omitted decompression (several minutes worth), but they should stay on the surface and breathe oxygen. Preparations should be made to transport to a recompression facility if signs and/or symptoms develop.

If one of the divers was symptom-free when he went back down, that was most likely not a good idea. [It is not clear to me the actual events. Did one diver actually have clinical DCS or simply omitted decompression?]

Dr Deco :doctor:

References :book3:

Koch AE, Kampen J, Tetzlaff K, et al. Incidence of abnormal cerebral findings in the MRI of clinically healthy divers: role of a patent foramen ovale. Undersea Hyperb Med. 2004 Summer;31(2):261-8. German Naval Medical Institute, Kiel-Kronshagen, Germany.

BACKGROUND: To investigate incidence and number of abnormal cerebral
hyperintensities (ACFs) in Magnet Resonance Imaging (MRI) and its relation to a
patent foramen ovale (PFO) in divers with no history of decompression illness.

METHODS: Cohort study on 50 divers (21-5500 dives).

MAIN OUTCOME MEASURES: Incidence and number of ACFs visualized by cranial MRI and presence and size of a PFO as documented by echocardiography and transcranial Doppler ultrasound (TCD) with echocontrast.

RESULTS: A total of 137 ACFs was found in the 50 subjects, with a significant correlation between the number of dives and number of ACFs (r = 0.28; p < 0.05); but after correction for age, the remaining correlation (r = 0.15) did not reach significance. In 18 divers, a PFO was present by either the application of echocardiography or TCD; in 12 divers, the PFO was of high hemodynamic relevance. Ten of 18 divers with a PFO had at least one ACF, while in the remaining 32 divers, only 14 had at least one ACF (56% versus 44%, p = NS). Seven of 14 divers (50%) with 4 ACFs had a PFO, compared to 11 of 36 (31%) with less than 4 ACFs (p = NS).

CONCLUSION: In this cohort of healthy divers, in contrast to an earlier report, no significant association was found between PFO presence and incidence or number of ACFs.

= = = = =

Blogg SL, Loveman GA, Seddon FM, et al. Magnetic resonance imaging and neuropathology findings in the goat nervous system following hyperbaric exposures. Eur Neurol. 2004;52(1):18-28. Epub 2004 Jun 22. Department of Environmental Physiology, Karolinska Institute, Stockholm, Sweden.

Divers may be at risk of long-term CNS damage from non-symptomatic hyperbaric
exposure. We investigated the effect of severe, controlled hyperbaric exposure
on a group of healthy goats with similar histories. Thirty goats were exposed to
various dive profiles over a period of 5 years, with 17 experiencing
decompression sickness (DCS).

Brains were scanned using magnetic resonance (MR) imaging techniques. The animals were then culled and grossly examined, with the brain and spinal cord sent for neuropathological examination.

No significant correlation was found between age, years diving, DCS, or exposure to pressure with MR-detectable lesions in the brain, or with neuropathological lesions in
the brain or spinal cord. However, spinal scarring was noted in 3 animals that
had suffered from spinal DCS.

 

[perche]

Hello,

Thanks Doc for the answers.

I will state my question more accurately because in fact MRI hyperintensities should be not understood as the purpose of my thread.

If one of the divers was symptom-free when he went back down, that was most likely not a good idea. [It is not clear to me the actual events. Did one diver actually have clinical DCS or simply omitted decompression?

Diver1 and 2 were symptom-free when they re-enter the water.
Diver1 made an in-water recompression to 9m depth surrounded by two people, with O2 and within 2minutes. Not clear what kind of symptoms he has after the in-water recompression. He was rushed to the hospital and get out 3 hours later. No HBO.
Diver2 3m depth, air, interval surface 9minutes. He didn’t want to go to this hospital. He made some phone calls and get two answers:
1) in-water recompression: bad idea! HBO
2) in-water recompression: bad idea! O2 during 2 hours.

Anyway one week later the two divers were always free of symptoms

It is my understanding (and my personal belief) that divers should not re-enter the water for omitted decompression (several minutes worth), but they should stay on the surface and breathe oxygen. Preparations should be made to transport to a recompression facility if signs and/or symptoms develop.

Depth was 55-57m.

In case of fast ascent or omitted stop nuclei grow to a sufficient volume to reach a point where silent or micro cerebral infarcts could happen (with perhaps long term effects) or DCS develop.

In case of fast ascent or omitted stop why we should wait for symptoms before going to recompression facility?

In case of fast ascent or omitted stop why we should not get (always) HBO as precaution?

what is the policy in US?

Thanks and Regards

 

[Dr Deco]

Hello perche:

Omitted Deco

1. The generality of decompression tables is that they are very conservative with respect to the safety margin. Therefore, DCS will generally not develop with some omitted decompression.

2. It is felt that signs and symptoms will not develop in most cases. For in-water repress, divers generally make very hasty provisions for re-descent, and this has lead to greater problems [e.g., death] than the omitted decompression.

3. Surface oxygen is a good alternative . Provision should be made for transport to a medical facility in case clear DCS develops. Most likely it will not, but it is a good safety precaution. I believe that DAN experience demonstrates this.

Fast Ascent

1. There is no doubt that too rapid an ascent will allow micronuclei to grow, possibly beyond the point where surface tension will keep them small. This is true. Nevertheless, problems still will not always appear because of the conservative nature of tables.

2. I would suggest that in cases such as these, effort should be made to remove the diver from the water with as little physical effort as possible on the part of the diver. Remove the heavy gear and assist him/her onto the boat . Do not let the diver climb aboard with all of the heavy gear, as this will also cause nuclei formation and growth.

3. There does not exist laboratory data on divers and omitted deco and exercise. This is an extrapolation from other studies. Therefore I cannot promise a wonderful ending – but that is what I would do.

4. If there are not any clear signs of DCS, HBO is probably not required, since there is nothing to treat. I definitely would not dive again for several days.

Dr Deco :doctor:

Readers, please note the next class in Decompression Physiology is September 10 – 11, 2005 :1book:
http://wrigley.usc.edu/hyperbaric/advdeco.htm

 

[perche]

Hello Dr Deco,

Thanks for your answer but let me express another opinion.

Diver 2 made some phone calls and get two answers:
1) in-water recompression: bad idea! HBO
2) in-water recompression: bad idea! O2 during 2 hours.

Answer 1 comes from a physician in charge of a recompression facility
Answer 2 comes from a well known diving organization/insurance.

To my knowledge, these bright areas [“T2-weighted hyperintensities” or “abnormal cerebral hyperintensities”] have not been shown to correlate with diving and DCS, in particular. (I believe that is what you mean by UFOs.) I have included recent references below that relate an increase in the number of bright areas with the presence of a PFO.

As far I know every radiological exam has false-positive or false negative results. Sometime «scientific studies» are also flawed by their design and the lack of gold standard.

Until now I believe there is not enough data to get an answer to this question. So that I’m not sure if we are able to talk about «long-term CNS damage from non-symptomatic hyperbaric exposure».

As a matter of fact every physician know about «silent» lesion of brain and spinal cord tissue. Maybe it never happens in case of diving accidents and incidents ??? !!!!

Recently 3T magnet appear on the market and perhaps like in MS we will see more lesions....

There is no doubt that too rapid an ascent will allow micronuclei to grow, possibly beyond the point where surface tension will keep them small. This is true.

OK !

Nevertheless, problems still will not always appear because of the conservative nature of tables.

Diver2 planned his dive with decoplanner or gap. Both said : «these software can kill you» . And to work with theses soft you have to answer : «I agree». I don't know if tables give you more guarantee to stay alive!

There does not exist laboratory data on divers and omitted deco and exercise.

So that in case of fast ascent the decision « not to treat » is a bet.

If there are not any clear signs of DCS, HBO is probably not required, since there is nothing to treat

Can I put it another way ?
We wait for symptoms.
DCS appears abruptly.
The course is unpredictable
Tetraplegia develops.
As far I know there is no guarantuee that «symptoms» resolve after treatment.
And perhaps the diver got irreversible neurologic deficits…..

We should forget about the cost of the treatment (source of conflict of interest) and avoid to play «russian roulette».

Just my two cents.

Best regards

 

[MikeFerrara]

I'm not sure that I'm following all of this but there is a difference between in-water recompression when there are symptoms and procedures for dealing with ommited decompression.

Gas supply and other conditions permitting I would absolutely go back down to do missed decompression provided that there were no symptoms and the decompression owed is significant. This is, in fact, consistant with what most technical agencies teach. While it's recommended that recreational divers stay out of the water after a screw up the omitted decompression is usually minimal and the diver is likely without the skill or equipment for staged decompression in the first place. The risk may also be minimal because we're likely talking about a few minutes of skipped decompression according to a conservative table. In contrast, a technical diver on a botched staged decomression dive may owe LOTS of decompression and he should be equiped and already know the numbers. If he doesn't do that decompression being bent is likely pretty close to a certainty and it might be the kind of bend where you aren't even going to make it to the chamber.

If there are symptoms I'd get on O2 and head for a chamber. In cases of remote areas where there is no chamber in-water recompression has been used successfully but the risks are obvious. If this is going to be considered O2, full face masks, slings and in-water support should be in place.

 

[perche]

Hello MikeFerrara

Thanks for this interesting comment

there is a difference between in-water recompression when there are symptoms and procedures for dealing with ommited decompression.

You’re right.

It is unclear with diver1 if we deal with «omitted decompression» or «in-water recompression», because O2 was given. An helicopter was on the scene but no diver (1 or 2) was rushed to a facility recompression. Diver 1 was sent to hospital.

With diver 2, it seems to me we deal with «omitted decompression». But Diver2 didn’t follow the rules ( he has to swim to the boat near the shore, to take a tank so that the intervalle surface is 9 minutes)

Anyway the two divers made a very fast ascent from 55-57m depth (one to call help, the other because he runs out of air)

And remind you :

There is no doubt that too rapid an ascent will allow micronuclei to grow, possibly beyond the point where surface tension will keep them small. This is true.

Gas supply and other conditions permitting I would absolutely go back down to do missed decompression provided that there were no symptoms and the decompression owed is significant. This is, in fact, consistant with what most technical agencies teach. While it's recommended that recreational divers stay out of the water after a screw up the omitted decompression is usually minimal and the diver is likely without the skill or equipment for staged decompression in the first place. The risk may also be minimal because we're likely talking about a few minutes of skipped decompression according to a conservative table.

In case of very fast ascent you can get pneumothorax, air embolism,… and I’m not sure it’s a good idea to go back in the water.

In contrast, a technical diver on a botched staged decomression dive may owe LOTS of decompression and he should be equiped and already know the numbers. If he doesn't do that decompression being bent is likely pretty close to a certainty and it might be the kind of bend where you aren't even going to make it to the chamber.

We deal with someting between recreationnal and tek diving. A max depth 57m and a decompression time about 15 min was planned.

Anyway I was a little bit amazed by the discrepancy between the approach to this problem by two specialized physician (one is in charge of a recompression facility, the other belongs to a well known diving organization/ insurance).

But until now I don’t know what we call "a fast ascent" !


Best regards

 

[Dr Deco]

Hello perche:

As far as I can tell, the two answers different in the administration of surface oxygen. If one physician recommended transport to a HBO facility and NOT breathe oxygen during transit, that is less than the best first aid treatment.

The second physician probably recommended surface oxygen and make plans to reach a hyperbaric facility if things do not turn out optimally.

Dr Deco :doctor:

Readers, please note the next class in Decompression Physiology is September 10 – 11, 2005 :1book:
http://wrigley.usc.edu/hyperbaric/advdeco.htm