Dysbaric Osteonecrosis Part 1

Will ‘diver’s rotting bone disease’ become more common as technical diving grows in popularity? 

By Dr. David Sawatzky

Dysbaric osteonecrosis (DON) was first identified in the 1940s and was found to be relatively common in the 1970s and early 1980s in some groups of divers but extremely rare in recreational divers.  However, recently I’ve become concerned that changes in the type of diving being done by recreational divers and the rapid expansion of technical diving will result in DON becoming more common in these groups.

Osteonecrosis simply means “bone death” and there are more than 30 causes.  Aseptic necrosis means that the bone is not infected (infected bone also becomes necrotic) and the table lists some of the causes.

Dysbaric osteonecrosis (“bone death due to bad pressure changes”) is of interest to divers.  There are many terms that have been used to refer to “pressure-induced bone death”, including “caisson arthrosis”, “caisson disease of bone”, “hyperbaric osteonecrosis”, “barotraumatic osteoarthropathy”, “avascular necrosis of bone”, “ischemic necrosis of bone”, “aseptic necrosis of bone”, “diver’s bone rot”, and “diver’s crumbling bone disease”.  Dysbaric osteonecrosis is the most accurate and commonly used title.

DON can develop in anyone who is exposed to changes in pressure and is therefore of concern to caisson workers (those who work in pressurized spaces used in building tunnels, bridge pilings, etc.), divers, aviators, and astronauts.  Caisson workers have been plying their trade longer than the other groups and our initial knowledge of DON was from this industry.

Background

In 1888, Twynam suggested that the areas of dead bone often seen in caisson workers were caused by pressure.  In 1913, Bassoe suggested that DON was somehow related to decompression sickness (DCS) as he noticed that caisson workers who had been bent were more likely to have DON.  In 1931, the Royal Navy submarine HMS Poseidon had an accident and five men were trapped at 120 feet (38 meters) seawater pressure for two to three hours before they escaped to the surface.  All five developed DCS soon after surfacing.  Twelve years later three of the five had x-rays taken. All three had DON, one with partial collapse of both femoral heads (the other two could not be located and x-rayed).  None of the five were divers or had other known pressure exposures.  This is very strong evidence that DON can develop from a single exposure to pressure.

The first reported case of DON in a diver was in 1941 and in 1943 Taylor noted a delay of several months from the pressure exposure that caused the DON to the observance of DON on x-ray.  About this time we also learned that DON was more common in caisson workers who had been exposed to higher pressures but could develop following exposure in caissons to as little as 17 psi (38 fsw or 11.6 msw) pressure.  DON was not seen in caisson workers who had worked only in caissons at lower pressures.  A 1972 study found DON on x-rays of 19{c383baab7bef8067e8c9786a45d8006c492489841a98fe37723e304bb1ddd030} of all caisson workers and 60{c383baab7bef8067e8c9786a45d8006c492489841a98fe37723e304bb1ddd030} of caisson workers with more than 15 years experience.

Several cases of DON have been documented in aviators but it is very rare and typically only seen in aviators who have suffered severe DCS that was not treated.

The frequency of DON in divers is more confusing.  The table below lists the findings of several studies.  These studies seem to suggest that the risk of DON is highest in divers who traditionally have the least amount of formal dive training, uncertain buoyancy control, and may have done insufficient decompression on their dives.  Other studies suggest that the groups with a high incidence of DON also have a very high incidence of DCS, and that it is often inadequately treated.

Diagnosis

How is DON diagnosed?  The most common way is through the use of x-rays.  On x-ray DON appears as a localized area of either increased or reduced bone density.  It is important to realize that x-rays only show the concentration of calcium salts in the bone and that if you take an x-ray of a bone from a person who has been dead for several months, you will not be able to tell it from an x-ray of a live bone.  In addition, the concentration of bone salts must increase or decrease by at least 50{c383baab7bef8067e8c9786a45d8006c492489841a98fe37723e304bb1ddd030} before the change can be seen on x-ray.  It takes at least three months and it may take as long as five years before DON lesions become visible on x-ray.  This makes it difficult to determine which pressure exposure(s) caused the damage, a fact that is very important to a litigious commercial diver trying to determine which of the companies he has worked for over the past few years to try to sue!  In addition, the area of change on x-ray is usually significantly smaller than the actual area of damage.  Finally, if the DON lesion is near a joint, x-rays do not allow us to predict which lesions will progress to collapse of the cartilage and subsequent destruction of the joint.

The Medical Research Council (UK) established a radiological classification of DON that is widely used.  They divided the lesions into those near joints (juxta-articular or A – lesions) and those in the head, neck and shafts of the long bones (B – lesions).

We now have several more sophisticated ways to look at dysbaric osteonecrosis. Bone scans involve venous injection of a radioactive material that is taken up by metabolically active bone.  The body is then scanned using a camera that detects radioactivity and areas of increased or reduced activity are identified.  In DON, the bone scan may be positive for increased activity (bone formation) within two to three weeks of the pressure exposure.  Interestingly, animal studies have detected the ischemia (no blood flow, reduced activity) of DON with bone scans within 24 hours of the pressure exposure.  The problem is that bone scans often detect lesions that never appear on x-rays (presumably because they heal normally, without a significant increase or decrease in calcium salts).  Conversely, the bone scan may become negative for a lesion that is visible on x-ray for the rest of the diver’s life.  To summarize, bone scans detect lesions that may not be significant and fail to detect some lesions that are significant.

We have limited experience with Magnetic Resonance Imaging (MRI) in DON.  It is generally more sensitive than bone scans but again, many of the lesions detected are probably not significant.  In addition, MRI is expensive and not widely available.

When osteonecrosis is found on x-rays, usually it is not possible to determine what caused the lesion.  The most common cause is trauma and the second most common is alcohol.  Therefore, when osteonecrosis is found in a diver, it might not be the result of diving!  In the next column I will finish discussing this fascinating condition.

Causes of Aseptic Necrosis

Decompression Sickness or dysbaric exposure
Steroid therapy or Cushing’s syndrome
Collagen diseases
Lupus erythematosus
Rheumatoid arthritis
Polyarteritis nodosa
Occlusive vascular disease
Diabetes mellitus
Hyperlipidemia
Liver Disease
Fatty liver
Hepatitis
Carbon tetrachloride poisoning
Alcoholism
Pancreatitis
Gaucher’s disease
Gout
Hemophilia
Polycythemia / marrow hyperplasia
Hemoglobinopathies (sickle cell)
Charcot joint
Specific bone necrosis disorders
Legg-Calve-Perthes
Kienbock’s
Freiberg’s
Kohler’s diseases
Radiotherapy