Descending Fast And Osteonecrosis

teomannaskali

Here is what I rememeber a medical doctor saying during my traning:

Although unproven descending too rapidly can cause osteonecrosis (bone death).

This is because the blood absorbs nitrogen fairly fast from the lungs creatnig a N2 concentration difference in the blood and the bone tissue (or any other tissue i would think). This difference in concentration sucks the fluids and nutrients in the bones just like salty water sucks non-salty water(Just like Osmotic pressure?).

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So we were advised to descend slowly.

Now with rebreathers, if you are prebreathing the rebreather with pure O2 then you are getting even more N2 out of your body. And if the period you stay on O2 is longer, the more N2 you get rid of (Which is good in Decompression sickness terms). But the above situation would seem to be amplified.


Does anybody have any info on this? What do you think? Or am I simply talking bollocks?


Teoman

Sutty

I can't imagine the N2 molecule is anywhere near large enough to have osmotic effects - but I stand to be corrected!

Neil

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Simon Mitchell

Hello,

Highly theoretical and never proven as a cause for dysbaric osteonecrosis. I would rate the evidence as insufficiently strong upon which to base recommendations on diving practice.

Nevertheles, the concept of gas induced osmosis is plausible, and is addressed by Brian Hills in the abstract pasted below.


Med Hypotheses. 1999 Mar;52(3):259-63.Related Articles, Links

A role for oxygen-induced osmosis in hyperbaric oxygen therapy.

Hills BA.

Paediatric Respiratory Research Centre, Mater Children's Hospital, Brisbane, Australia.

The principles of gas-induced osmosis, demonstrated in the 1970s, have been applied to the very large steady-state gradients of O2 arising between arterial blood and hypoxic tissue during hyperbaric oxygen (HBO) therapy to produce a fluid 'pump' in the desired direction for resolving accompanying oedema. Thus, in soft-tissue injuries, an oxygen-induced fluid pump would break the vicious cycle between ischaemia, hypoxia and oedema at the point of oedema rather than hypoxia, as hitherto assumed. This osmotic mechanism enables the successes of HBO therapy in hypoxic disorders to be reconciled with early failures in such areas as hyperbaric radiotherapy, where substitution of O2 for N2 in inspired air was clearly not reflected at the tissue level. This argument also applies to the success of HBO in treating air embolism and decompression sickness over simple compression. The oxygen pump would seem to offer a more plausible explanation for the success of HBO therapy than theories based upon O2 delivery by the circulation, especially when considering cardiovascular reflexes to elevated PaO2 and the marginal increase in blood O2 content upon switching to HBO from normobaric oxygen breathing. Hope this helps.

Simon M

Joe Botz

i read (aproxx. 16 yrs. ago) ,,,just found the book,,,,deeper into diving by John Lippman,,, said book has some interesting info pertaining to Dysbaric Osteonecrosis..
it is a good book I'll try to read the chapter and report back.

what I recall is that gas bubbles occlude the blood flow,or that possibly platlets attach themselves to said bubbles,,including "micro/silent bubbles."

as diving continues areas of the body ie. retinas, bones etc. eventually sucome to this action,,causing decreased blood flow in areas and causing tissue to become necrotic.

also o2 toxicity might have an effect,,nitrogen is also very soluble in the fatty bone marrow.

the indcidence of dysbaric osteonecrosis appears to be greater in divers who:

spend long times underwater
have been diving for many years
dive deeper than a mere 100ft
undertake experimental diving
have suffered from bends, especially if inadequately
are fatter or heavier

ScubaDadMiami

This doesn't make sense to me. Although the PPN2 is increased during descent, so is the PPO2. So, there would seem to be adequate O2 supply arriving at the bones during descent and on the bottom.

The only time it would seem to make sense for necrosis to occur would be during ascent, when N2 bubbling could form due to inadequate decompression, thus blocking the tissues from receiving adequate oxygen supply.

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AD_ward9

Interesting thread, and Joe's post has done a good job in ignoring the tripe: the rate at which rebreather divers descend, to avoid PPO2 spiking, is so slow that I cannot see quick descents as an issue.

Wrong decompression is a much bigger issue: bone is reported to have a 10 hour half life, which none of the common dive algorithms support. The reason for the long half life is bone has very small blood vessels, so gases diffuse out really slowly, and you only need a really small bubble to block them.

Incidentally, bone death is quite painful because in divers the bones in the joints die first.

I will post a picture in the next day or two from a recent X-rax to keep track of the various bits of my body that ache, to show what it looks like (black streaky areas in the ends of bones in X rays).

Anyone who has suffered diving with me can testify that I am never the first on the sea bed unless I have forgotten to plug in the dil , so fast descent is not the cause. Not fat or heavy either. Duff deco algorithms is the likely cause. As we do longer dives, this long half life tissue compartment is something to treat with care.

Cheers,
Alex

AD_ward9

Here is the picture I promised, of one of the joints with diagnosed osteonecrosis. X-ray pics do not scan well: lots of black whereas the pic on a light box shows much more detail. Anyhow, I stuck an arrow on one of the dark bits where where the specialist said it was osteonecrosis. Light box shows like a spider of black areas that are just black on the scan.

Just to underline, if involved with deep, long or experimental diving, give enough time for your bones to decompress.

Alex

Attached Images

Joint_1A.jpg (59.5 KB, 97 views)

babar

FWIW the best way to digitalize your xrays is to take a photo (no flash) while on the light box. I cant quite make out what part it is, but what you see in the xray is a local loss of the dense cortical bone (white) with a small defect.


Heres another example. This is an MRI, imagine someone sliced in half front to back.
Here's a link to an article on medscape: http://www.medscape.com/viewarticle/408486_5

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