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Dysbaric Osteonecrosis Part 2

It’s rare in the recreational scuba enthusiast but deeper divers and pushing no-decompression limits can put you at risk


By Dr. David Sawatzky

The lesions of dysbaric osteonecrosis (DON) only occur in a few bones of the body.  They are found in the head and proximal shaft of the humerus (shoulder), the head of the femur (hip), the distal shaft of the femur (above the knee), and in the proximal shaft of the tibia (below the knee).  In general, divers are more likely to develop DON in the shoulders and caisson workers more likely to develop DON of the hips.  However, in Japanese Shell Fishermen the hips are involved relatively frequently.

What are the symptoms of DON?  For all lesions there are no symptoms initially and for head, neck and shaft lesions there are never any symptoms.  The diver is not aware of the lesions; they are only found on routine x-rays.  For juxta-articular lesions (meaning next to joints – see Table) there are no symptoms initially; however, there is usually significant pain when the lesions collapse and, after arthritis develops, there can be almost continuous, severe discomfort.  Juxta-articular lesions virtually never develop near the knee.

How do we monitor DON?  The only practical way is with routine x-rays.  The standard is to do a single anterior-posterior view of each shoulder, each hip and a lateral view of each knee, including the adjacent bones in all cases (6 pictures total).  This series is called a Long Bone Survey (LBS).

The Canadian Forces (CF) does a LBS on all divers after they finish their initial diving course to establish the existence of any lesions that might be present (and therefore not due to diving in the CF).  They do not x-ray before the course because a fair number of students will fail and never dive again and because the type of diving done on the course does not cause DON [maximum depth 100 fsw (30 msw)].  When CF divers leave the military they should have a LBS to document whether they suffered osteonecrosis during their career (in a perfect world, the x-rays would be done at least six months after the last military dive).

DON and Depth

What kind of diving has an increased risk of DON?  We know that if the maximum depth to which a bounce diver is exposed is less than 100 fsw (30 msw), there is essentially no risk of developing DON.  For bounce divers whose maximum depth is 100 to 165 fsw (30 to 50 msw), the lifetime risk is approximately 0.8 percent.  Duration of exposure is also important.  Commercial divers who accumulate up to six hours of bottom time per day at shallower depths on profiles where DCS occurs, also may develop DON.  We know that if all cases of DCS are treated with current treatment tables, there is a very low risk of developing DON.  Therefore, it is not necessary to monitor most sport divers and most of you reading this column can now start to relax!

However, for divers who routinely dive deeper than 100 fsw (30 msw) and certainly for divers who regularly dive deeper than 165 fsw (50 msw), the LBS should be repeated every five years.

So what causes DON?  The short answer is that we do not know, but we have some ideas.  DON only occurs in bones that have a large fatty marrow compartment.  In other forms of osteonecrosis, and probably in DON, stasis of venous blood in the marrow leads to interruption of blood flow to some of the bone and that bone dies.

It has been postulated that fat embolism and platelet thrombi cause the damage by blocking the circulation in bones.  For years it was thought that bubbles caused by decompression stress blocked the circulation in divers’ bones and thereby caused DON.  However, this does not explain why DON seems to affect only some sites, nor why aviators (who have lots of bubbles) almost never develop DON.

From an animal model of DON we’ve found that DON is usually associated with increased intramedullary pressure and that fat cell necrosis in bone marrow has a strong link to DON.  We also have found that fat cells swell when exposed to increased partial pressures of oxygen and that divers with a history of exposure to a partial pressure of oxygen greater than 0.6 ATA for more than four hours have an increased risk of developing DON.  Therefore, is it possible that DON is a form of oxygen toxicity (since aviators are never exposed to high pO2)?  Although this might be a factor, I do not think this is the entire story.  The strongest argument against this theory is that divers and animals do not develop DON if treated with high pO2s (treatment tables) within eight hours of developing the signs or symptoms of DCS.

What Causes DON?

I think a more likely explanation of the pathophysiology of DON has to do with marrow.  Bone and bone marrow are very slow tissues with limited perfusion.  We know that DON does not develop in red marrow nor in bone that does not have marrow.  Divers and caisson workers who have been exposed to either 1) increased pressure for a significant period of time or 2) very high partial pressures of inert gas will have a significant inert gas load build-up in the fat cells of white (yellow) bone marrow. When the individual decompresses, bubbles are formed in the yellow marrow.  The blood supply of bone enters the marrow cavity and then goes back out to supply the bone.  The marrow cavity has a fixed volume and when bubbles form, they take up space.  This in turn causes a rise in intramedullary pressure.  If the pressure rises above the perfusion pressure of the marrow, the blood flow will stop.  We know that bone cells can survive for four to six hours without blood flow.

Therefore, for an individual to develop DON, inert gas supersaturation in the yellow bone marrow would have to be great enough that when the pressure was reduced, sufficient bubbles formed to cause the intramedullary pressure to rise above the perfusion pressure. That higher intramedullary pressure would have to be maintained for at least four to six hours to kill the bone cells.  Exposure to high partial pressures of oxygen would result in swelling of the fat cells in the yellow marrow and under these circumstances fewer bubbles would be required to raise the intramedullary pressure high enough to cause DON.  This explanation fits the known observations (still no guarantee that it is correct!).

Another theory is that a rapid rate of compression could be a factor.  Rapid compression impedes venous drainage of bones and could lead to intramedullary venous stasis.  Bubbles could also trigger a local inflammatory/thrombogenic response and increase the risk of DON as a result.  The bottom line is that DON is most likely a result of untreated or inadequately treated decompression stress/sickness.

Rare in Rec Divers

There is no treatment for DON once it has developed.  For head, neck and shaft lesions you must dive more conservatively, since you have “proven” that the decompression you have been doing is inadequate for you!  If you have a shaft lesion, your risk of developing a juxta-articular lesion is elevated.  The lesions should be checked occasionally with x-ray since there have been a few cases of malignancy (cancer) developing at the site of an osteonecrotic lesion.

Juxta-articular lesions are of much greater concern, as 10 to 40 percent of them will lead to collapse of the cartilage and destruction of the joint.  If the diver could rest the joint completely for several months the bone might heal, but often this is not practical.  Sometimes a bone graft is done to help the lesion heal but this does not have a good success rate.  The joint can be realigned so that pressure is taken off the damaged joint surface. This sometimes gives symptom relief.  When the joint collapses and the individual develops severe arthritis, the joint can be fused to control the pain or replaced with an artificial joint.  Unfortunately, artificial joints wear out and surgeons are hesitant to put them into young active divers.

What general conclusions can be drawn?  First, DON seems to be related to inadequate decompression and may be exacerbated by prolonged exposure to high partial pressures of oxygen and/or rapid rates of compression.  It is exceedingly rare in recreational divers.  For the normal, conservative sports diver DON is not a concern and even a baseline LBS is not required.  For those who push their decompression computers right to the no-D limit every time they dive and do a lot of relatively deep diving, DON might be a possibility. In this case, a LBS might be a good idea every five years or so.

For the technical diver doing very advanced dives or the diver who violates decompression tables or computers regularly, a LBS every five years is recommended.   If a diver develops decompression sickness (DCS) in the shoulder or hip, an x-ray one year later to check for DON is not a bad idea.

Discovery of a head, neck or shaft lesion suggests that the diver has been doing inadequate decompression.  These lesions almost never cause problems and if the diver continues to dive to less than 100 fsw (30 msw) and uses conservative decompression profiles, he or she is unlikely to experience difficulties.

The diver who develops a juxta-articular lesion has a 10 to 40% chance of the lesion collapsing.  The recommended course is to stop diving and rest the joint as much as practical for several months.

The good news in all of this is that since we started monitoring commercial and military divers for DON in the 1970s, we have found very few new cases.  Over the years, decompression procedures have become more conservative and safer.  We have far less DCS and DON than in the past.  Some militaries have stopped even screening for DON.

DON is highly unlikely in conservative sports divers but if you move into a form of diving where decompression procedures are not as well tested, the risk of developing both DCS and DON starts to increase.



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