osteonecrosis

[Makhno]

I'm curious about something I've noticed in the literature (in the Rubicon Foundation archive and elsewhere) about dysbaric osteonecosis (DON). Namely, why is it assumed that deep decompression diving by someone with DON may make the existing osteonecrosis worse?

There seems to be a lot of evidence that DON is caused by improper/inadequate decompression. E.g., "Investigators have related dysbaric osteonecrosis to a variety of factors involved in diving, but all factors ultimately relate to inadequate decompression" Wade et al., "Incidence of Dysbaric Osteonecrosis in Hawaii's Diving Fishermen" p. 138.

Sometimes the doctors advise DON patients (or at least those with "juxta-articular" or near-the-joint lesions) not to dive again. E.g., "We recommended that divers with Type A lesions stop diving", Toklo and Comsit, Dysbaric Osteonecrosis in Turkish Sponge Divers" p. 86; "Divers should avoid diving and strenuous exercise as soon as juxta-articular lesions are found", Yangsheng at al., "Investigation and Analysis of Dysbaric Osteonecrosis in 171 Divers" p.126. But see Bove, Bone Injuries From Diving (“My patient asked if he could continue diving. My response was that deep decompression diving was likely to make the osteonecrosis worse and might cause lesions in other joints. Shallow, no decompression diving is not likely to aggravate the damage already present.”)

So my question is: Why is “deep decompression diving … likely to make the osteonecrosis worse”? Why isn't the recommendation to dive with proper and adequate decompression, rather than not to dive again at all (or in the case of Bove's advice, only to do shallow no-stop dives)? In other words, if a diver with DON does deco stops according to tables derived from a conservative decompression model – and pads the stops for extra conservatism – then why might that exacerbate the DON? Is the assumption that there is still some persisting blockage of the veins and capillaries, even though the dives causing the DON may have been years ago? A related question is: Why should doing conservative deco-stop diving be inherently riskier than doing shallow diving? -- because after all, even shallow diving generates some silent bubbles. Seems to me that if the deco is conservative enough, then the depth and time aren't so important; what's assumed to be important is the presence/size/number of bubbles, correct?


Thanks in advance for whatever info you can share.

 

[Dr Deco]

Hello Makhno:

Dysbaric Osteonecrosis and Tables

Decompression tables are designed primarily to prevent joint-pain DCS. There is also the axiom that if this type of DCS can be prevented by the decompression scheme, then neurological DCS will also not appear. This is true at least in laboratory trials.

These forms of decompression sickness present shortly following the pressure decrease and thus can be easily identified. The table can be corrected. Dysbaric ON, in contrast, appears after several years of diving; a specific dive/decompression protocol can seldom be identified. Generally, it is thought that many dives over many years are needed for DON. Therefore, the terms “adequate decompression” or “suffice stops” are difficult to define for this diving malady.

Dysbaric Osteonecrosis and Deep Diving

Some decompression disorders do not appear unless the absolute pressure change is large enough. In altitude decompression, spinal forms of DCS are virtually nonexistent unless arterial embolism occurs [and even then it is rare]. Vestibular problems do not appear in attitude depress, and likewise DON.

I suspect that the reason is that the micronuclei in certain tissues are too small and cannot be enlarged without sufficient pressure changes. Recreational diving has [relatively] small pressure changes and short tissue gas loading times, at least in tissues responsible for DON, and it does not appear.

From this we might suspect that some types of diving [e.g., deep] will cause DON problems or exacerbate those already present. Difficulties arise in determining cause since osteonecrosis can appear in nondivers. It is most commonly brought on by steroids and hard drinking. Professional divers are known to be hard drinkers thus cofounding the cause – or causes.


Dr Deco :doctor:

 

[Makhno]

Thanks, Dr. Deco, for the reply.

Just to clarify, though: the concern about deep diving exacerbating existing DON is about inadequate deco (however defined) happening again on those post-diagnosis dives, and resulting venous/capillary occlusion happening again, correct?

In other words, there's no assumption that there's any occlusion persisting from the previous DON-causing dives? Nor any other means or mechanism by which the presence of ON itself somehow makes deep diving inherently riskier by ON patients than by non-ON patients?

Thanks again; very interesting.

 

[DocVikingo]

Hi Makhno,

There is still much to be researched regarding DON.

While it can occur in humans and animals following a single hyperbaric air exposure with inadequate decompression, it generally is thought to be a cumulative pathology of bone brought about by repeated episodes of large ambient pressure changes.

And while the hypothesis has a certain amount of intuitive appeal, it in fact is not clear that inert gas occlusions in the osseous vasculature are the cause of DON. Abnormal lipid and platelet aggregates have been found in bone marrow tissue following seriously mismanaged decompression. It is therefore possible that rapidly expanding inert gas bubbles precipitate fat emboli, hemoconcentration and increased intravascular coagulation, and that these cause the observed obstructions.

Regards,

DocVikingo

 

[DocVikingo]

...there's no assumption that there's any occlusion persisting from the previous DON-causing dives? Nor any other means or mechanism by which the presence of ON itself somehow makes deep diving inherently riskier by ON patients than by non-ON patients?

For the clarity of discussion:

ON=osteonecrosis, which can have all manner of causes, including trauma, drug, blood disorder and autoimmune disorder.

DON=dysbaric osteonecrosis, which is specifically associated with exposure to large ambient pressure changes.

"deep diving" -- the risk really isn't simply deep diving per se. It's risky inert gas loadings, no matter how they are acquired, coupled with improperly managed decompression.

As to your question, whether or not an intravascular occlusion persisted from "previous DON-causing dives," unless only partial occlusions are being hypothesized the damage from a blockage has already occurred---the tissues previously oxygenated via the involved vessels are now necrotic. New occlusions related to SCUBA can't make them any more dead. In the case of only partial occlusion (which, given the caliber/gauge of the blood vessels involved, seems highly unlikely), yes, it theoretically would be possible that additional emboli could complete the existing obstruction and cause additional harm.

As an aside, occlusions in the form of actual inert gas bubbles certainly do not persist for but a very brief duration (although their effects do). Those composed of abnormal lipid and platelet aggregates would persist for longer, but most likely couldn't be detected in and of themselves by the next time one formally looked for them.

As regards "other means or mechanism by which the presence of ON itself somehow makes deep diving inherently riskier by ON patients than by non-ON patients": It would seem that if an ON patient already had compromised bone, such as in the upper or lower femur, upper
humerus, upper tibia or other joint, then exposing that patient to potential SCUBA-related DON would seem to be increasing risk.

Are we gaining on it, Macky?

Regards,

DocVikingo

 

[Makhno]

Thanks DocVikingo,

What you've said makes sense and accords with my layperson's understanding of what I've read in the medical literature.

The proposition I quoted above that “deep decompression diving [is] likely to make the osteonecrosis worse” (emphasis added) doesn't make sense to me, hence my query here on scubaboard.

But you set forth a quite different proposition, which does make sense to me: "It would seem that if an ON patient already had compromised bone ... then exposing that patient to potential SCUBA-related DON would seem to be increasing risk," and that the risk arises from "risky inert gas loadings ... coupled with improperly managed decompression." That makes a lot more sense.

Thanks to both docs for your replies.

 

[Dr Deco]

Hello Machno:

It is not clear exactly the pathway for DON. As Dr Vikingo mentions, this malady has occurred with just one bad decompression. Thus repeated embolizations are not always necessary, apparently. [And we also have steroids and alcohol use. ]

In some individuals, DCS occurs more easily than in other divers, probably because they are prone to bubble formation [whatever that process might be]. I can certainly guess that some divers could be more prone to bubble formation in or near bone. These bubbles, or their sequelae such are cell aggregation, could occur more readily. This is addition to exacerbating the lesion already present.

Since the dive and the DON are often separated by months, or years, the actual causative dive might be hard to pin down.

Dr Deco :doctor:

 

[Cruisin Home]

Just my medical/scientific thought is that there is most likely a vascular based reason for this disiease state. Whether it be DCS, alcohol, steroid, radiation, etc. likely casuing permanent vasoconstriciton/stenosis, maybe at the capillary level to bone in question. Lot harder to vascularize bone, supposedly a new bone cement coming out that has a component that helps to regrow the vasculature faster, particlarly in large non-union type fractures. I'd like to think as far as the diving based cause that it probably only occurs in violation/abuse of deco tables.

 

[DocVikingo]

Of interest:

"Undersea Hyperb Med. 2010 Sep-Oct;37(5):281-8.

Dysbaric osteonecrosis in recreational divers: a study using magnetic resonance imaging.

Kenney IJ, Sonksen C.

Royal Alexandra Hospital, Eastern Road, Brighton, Sussex, United Kingdom. ian.kenney@bsuh.nhs.uk

Abstract

OBJECTIVE: We set out to identify whether magnetic resonance imaging (MRI) would identify evidence of dysbaric osteonecrosis (DON) in a group of experienced recreational scuba divers.

DESIGN: Local British Sub Aqua Club divers of at least Trainee Dive Leader grade were offered MRI scans (T1 and TIRM sequences) of hips, femora and shoulders. Anonymous images were interpreted separately by two radiologists, and cases not considered unequivocally normal were discussed for consensus opinion.

RESULTS: Of 26 divers imaged, five merited discussion. Four of these were considered to show unrelated normal variants or incidental findings. Only one case (abnormalities in the right humerus and left femur) could have possibly represented osteonecrotic lesions. After obtaining plain radiographs and more detailed clinical and dive history, these lesions were considered "indeterminate" but probably not DON by both reviewers and after taking further specialist musculoskeletal MRI opinion.

CONCLUSION: This study found no evidence that DON is a significant risk in recreational scuba diving and as such concurs with prevailing current opinion."

Regards,

DocVikingo

 

[Duke Dive Medicine]

Saturation divers are especially vulnerable to DON. Since they're very carefully decompressed, it seems likely that there is another contributing factor besides bubbles. There's been some interesting research on pressure and microparticles, and Thom & colleagues will be publishing another study soon.