Dysbaric Osteonecrosis

"Dysbaric means "bad pressure' osteo means 'bone' and necrosis means 'cell death'. Therefore dysbaric osteonecrosis is simply bone cell death as a result of pressure changes."

By Dr. Sawatzky

Last issue we started a discussion on dysbaric osteonecrosis. In this column we will conclude our discussion of this fascinating diving medical problem.

The lesions of DON are only found 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 British divers the lesions are most common in the shoulder, the distal femur and rare in the hips. Conversely, in caisson workers the hips are the most commonly affected site. In general, divers are more likely to develop DON in the shoulders and DON of the hips is rare. However, in Japanese divers the hips are involved almost 50% as often as the shoulders.

Bone islands are isolated areas of increased density commonly found on x-ray. They are not more common in divers and are of no significance. They are usually not even reported but if the radiologist mentions them and your doctor tells you some were seen on your x-rays, don't worry. They are not a result of diving and have no clinical significance.

One of the major problems with DON is that osteonecrosis from other causes is frequently found on x-rays and it is some times extremely difficult to tell what caused the lesion. The most common cause of osteonecrosis is trauma. For example, if you break the neck of the femur, even though it is set or pinned and seems to heal normally, the person will quite often develop an area of osteonecrosis in the head of the femur later. The next most common cause of osteonecrosis is alcohol. Of course, no diver drinks alcohol so if you find osteonecrosis in a diver you know that it must be due to diving (ya right)! Steroids are often used for medical problems and they have been shown to result in osteonecrosis in some individuals. Abnormalities of hemoglobin (sickle -cell anemia, thalassemia) have been shown to cause osteonecrosis and osteonecrosis is seen in many specific bone diseases (Perthe's disease, Kienbock's disease, Freiberg's disease, Kohler's disease, etc.). Unfortunately, the list continues. Osteonecrosis is seen in people suffering from systemic lupus erythematosus, pancreatitis, radiotherapy, radium therapy, and diseases of liver metabolism (Gaucher's disease, fatty liver, hepatitis, carbon tetrachloride poisoning, hyperlipidemia, diabetes, etc.). It is also seen in idiopathic avascular necrosis, rheumatoid arthritis, gout, neurosyphilis, syringomyelia, alkaptonuria, arteriosclerosis, sarcoidosis, syphilis, etc. O.K. Finished. As should be very obvious by now, if a diver is found to have osteonecrosis, the cause is not always diving!

What are the symptoms of DON? For head, neck and shaft lesions, there are no symptoms. The diver has no awareness of the lesions and they are only found on routine x-rays. For juxta-articular lesions (next to joints) there are no symptoms initially but there is usually significant pain when the lesions collapse and, after arthritis develops, the diver can be in agony.

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. Full inspiration and expiration chest x-rays are often done at the same time to look for lung problems. What kind of diving has an increased risk of DON? We know that if the maximum depth a bounce diver is exposed to is less than 30 msw (100 ft), they have essentially no risk of developing DON. For bounce divers whose maximum depth is 30 to 50 msw (100 to 165 ft) the lifetime total risk is approximately 0.8%. Time of exposure is also important. Commercial divers who accumulate up to six hours of bottom time per day at shallower depths, on profiles where persistent limb bends (untreated) occur, also develop DON. We know that if all cases of DCS are treated with current treatment tables, there is almost no risk of developing DON. Therefore it is not necessary to even monitor most sport divers and most of you reading this column can now start to relax!

The Canadian Forces does a set of x-rays (long bone survey) on all divers after they finish their initial diving course to establish the existence of any lesions that were present before they started diving. They do not x-ray before the course because a fair number of students will fail and never dive again, because the type of diving done on the course does not cause DON, and because it takes at least three months for the lesions to develop. Therefore, even if the student suffered a bone injury on the course, it would not show on the initial x-rays. For divers who routinely dive deeper than 30 msw, the CF currently repeats the x-rays every three years but that may soon be reduced to every five years. If a diver suffers from DCS, the affected joint should ideally be x-rayed every year for three years afterwards to look for DON. Finally, when a CF diver leaves the military they receive a set of long bone x-rays to document whether they have suffered DON during their career (in a perfect world, the x-rays would be done at least six months after the last military dive).

So what causes DON? The short answer is that we do not know. However, there are several theories and some interesting data is becoming available now that Dr. Charles Lehner of the University of Wisconsin has developed a good animal model of DON. Much of the research we need to understand diving medical problems has to be done on animals because no ethics committee would approve the necessary experiments using humans. Of course there are some that would argue divers aren't human anyway!

For some of the non-diving DON, it has been postulated that fat embolism and platelet thrombi cause the damage by block ing the circulation in bones. For divers, it has been believed for years that bubbles caused by decompression stress blocked the circulation in bones and thereby caused DON. This does not explain why DON only seems to affect some sites nor why aviators (who have LOTS of bubbles) seldom develop DON.

We now know that DON is usually associated with increased intramedullary pressure and that fat cell necrosis in bone marrow will result in DON. We also know 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 (aviators are never exposed to high pO2s)? 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 who are treated with high pO2s (treatment tables) within eight hours of developing the signs or symptoms of DCS do NOT develop DON.

My best guess and 'Lehner's Hypothesis' (Dr. Lehner reviewed these two columns for me) as to the pathophysiology of DON goes as follows. Bone and bone marrow are very slow tissues with limited perfusion. Therefore, divers and caisson workers must be exposed to increased pressure for a significant period of time or they must be exposed to very high partial pressures of inert gas so that a significant inert gas load can build up in the fat cells of white (yellow) bone marrow. We know that DON does not develop in red marrow nor in bone that does not have 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 the bone cells can survive for only four to six hours without blood flow. Therefore, to develop DON we would need to have enough inert gas supersaturation in the yellow bone marrow so that when the pressure was reduced, enough bubbles would form to cause the intramedullary pressure to rise above the perfusion pressure. We would then have to maintain that pressure for at least four to six hours to kill the bone cells. An exposure to high partial pressures of oxygen would simply result in some swelling of the fat cells in the yellow marrow and therefore, 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!).

The treatment of DON once it has developed is pretty simple, there isn't any (remember early treatment of DCS will prevent DON from developing). For head, neck and shaft lesions you must simply dive more conservatively as you have proven that the decompression you have been doing is inadequate, for you! It is also worthwhile to follow the lesions occasionally with x-ray, as there have been a few cases where a diver developed a malignancy (cancer) at the site of an osteonecrotic lesion. For juxta -articular lesions where destruction of the joint is possible, one option is for the diver to rest the joint for several months until it is healed (not practical). Sometimes a bone graft is done to help the lesion heal or the joint is realigned so that pressure is taken off the dead bone (sometimes works). When the joint collapses and the diver develops severe arthritis, the joint is often fused to control the pain or replaced with an artificial joint. The problem with artificial joints is that they wear out and surgeons are hesitant to put them into young active divers.

What general conclusions can be drawn? First, DON is a result of inadequate decompression and is exceedingly rare in recreational divers. For the normal, well-trained sports diver, DON is not a concern and even a basic set of x-rays is not required. For the technical diver doing very advanced dives or the diver who violates decompression tables or computers regularly, routine long bone x-rays are probably a good idea every five years or so. If a head, neck or shaft lesion is found, it proves that the diver has been doing inadequate decompression. These lesions almost never cause a problem and if the diver dives to less than 30 msw (100 ft) and uses conservative decompression profiles, they are unlikely to experience difficulties. For the diver who develops a juxta-articular lesion, they have a 10 to 40% chance of the lesion collapsing. Therefore, they should probably stop diving and rest the joint as much as possible 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 less DCS and far less DON than in the past. Just remember, DON is highly unlikely in well-trained 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.