aseptic bone necrosis

[oldmossback]

Doc

Would you please explain Aseptic Bone Necrosis, how it affects ones bones and what the symtoms are? Was slightly bent diving in my youth approx. 36 years ago. Some noticeable ache in my right hip joint then. No recompression treatment done, and the ache went away after a few days. Having some issues with my right hip joint now. Would like to rule out necrosis if possible.

OldMossBack

 

[H2Andy]

here's a quick read for you (this is a quote from the article):

Capillary Atrophication and Aseptic Bone Necrosis

Perhaps the best known of the long term problems is Aseptic Bone Necrosis, where the destruction of capillaries within bone tissues causes local necrosis of the bone - that is, the bone tissue effectively dies and falls apart. Traditionally, the long bones (thighs, shins, arms) were most at risk, with the heads of joints at shoulder and pelvis especially at risk. At one time this was though to occur primarily in commercial saturation divers, but it has been fairly commonly recorded in recreational divers, where there is some evidence to suggest that it affects the center sections of bones rather than the ends. What causes it is not entirely known, other than it is associated with capillary Atrophication. Such Atrophication may be associated with rapid pressurization and/or depressurization, where different tissues within the bloodstream on and offgas at different rates. This means that certain of the blood's constituent tissues may at different times during descent or ascent act as effective dams within the smallest capillary beds, creating tiny local embolisms or micro-Atrophication. Though this is perhaps most crucial in bones, capillary beds also exist in other vital areas of the body such as the brain, soft tissues such as the liver, kidneys, eyes, etc. At present, alterations to capillary bed structure in these other tissues are best described as "change" rather than damage, until more research is done on both cause and effect.

Research on Aseptic Bone Necrosis shows that affects approximately 5% of divers (both recreational and commercial) to some degree or another. Deep mixed gas diving may be one contributory factor, as may rapid pressurization/ depressurization, but the increase in symptoms evinced in recreational divers who do not undertake such practices suggests that the problem still warrants further research before too many conclusions can be drawn.

http://www.abysmal.com/web/library/articles/physiology_and_pysics_of_helium.html

 

[oldmossback]

here's a quick read for you (this is a quote from the article):

Capillary Atrophication and Aseptic Bone Necrosis

Perhaps the best known of the long term problems is Aseptic Bone Necrosis, where the destruction of capillaries within bone tissues causes local necrosis of the bone - that is, the bone tissue effectively dies and falls apart. Traditionally, the long bones (thighs, shins, arms) were most at risk, with the heads of joints at shoulder and pelvis especially at risk. At one time this was though to occur primarily in commercial saturation divers, but it has been fairly commonly recorded in recreational divers, where there is some evidence to suggest that it affects the center sections of bones rather than the ends. What causes it is not entirely known, other than it is associated with capillary Atrophication. Such Atrophication may be associated with rapid pressurization and/or depressurization, where different tissues within the bloodstream on and offgas at different rates. This means that certain of the blood's constituent tissues may at different times during descent or ascent act as effective dams within the smallest capillary beds, creating tiny local embolisms or micro-Atrophication. Though this is perhaps most crucial in bones, capillary beds also exist in other vital areas of the body such as the brain, soft tissues such as the liver, kidneys, eyes, etc. At present, alterations to capillary bed structure in these other tissues are best described as "change" rather than damage, until more research is done on both cause and effect.

Research on Aseptic Bone Necrosis shows that affects approximately 5% of divers (both recreational and commercial) to some degree or another. Deep mixed gas diving may be one contributory factor, as may rapid pressurization/ depressurization, but the increase in symptoms evinced in recreational divers who do not undertake such practices suggests that the problem still warrants further research before too many conclusions can be drawn.

http://www.abysmal.com/web/library/articles/physiology_and_pysics_of_helium.html

Ok, thanks for the update, but what are the symptoms if any.......suggested medical testing for this problem? The local landlocked doc's I've been to are not up on this issue.

 

[H2Andy]

i don't know, sorry... i did a google search and came up with that article

have you tried talking to DAN? they can set you up with a local physician
who understands diving:

1-800-446-2671

or 1-919-684-2948

 

[ScubaDadMiami]

I believe that they can test for this. Not sure if it is x-ray, MRI or CT Scan, but I believe that this can be found out pretty easily. I am not a physician. So, check into it from someone who knows.

 

[John C. Ratliff]

OldMossBack,

I'm the guy who sent you here from the vintage scuba web site, but I post on both sites. I did not want to comment at the time as I did not have the reference in front of me on osteonecrosis. When I worked for Oregon OSHA (then the Accident Prevention Division) in the 1970s, I was given this reference. It is titled:

DYSBARISM-RELATED OSTEONECROSIS
Proceedings of a Symposium on Dysbaric Osteonecrosis
Presented by the
Marine Biomedical Institute
The University of Texas Medical Branch
Galviston, Texas
February 1972

Scientific Editors
EDWARD L. BECKMAN
DAVID H. ELLIOTT

U.S. DEPARTMENT OF HEALTH, EDUCATION, AND WELFARE
Public Health Service
Center for Disease Control
National Institute for Occupational Safety and Health
1974

There are several quotes that may help you decide what's going on. Here they are:

PREFERENCE

The industrial Revolution not only increased man's creature comforts, but also his liability to industrial diseases. Onec such disease is osteonecrosis related to decompression sickness, or dysbarism.

Osteoneecrosis has long been recognized as secondary to other disease processes--e.g., sickle-cell anemia or fracture of the neck of the femur. But it was only when man began exposing himself to large changes in ambient pressure, such as in flying, diving, and working in a caisson, that he learned about decompression sickness. Even more recently he learned that osteonecrosis is one aspect of this perplexing disease of dysbarism. Osteonecrosis thus caused may be considered a chronic form of the disease; it may be debilitating and ivaliding as well. This disease is therefore of vital concern whenever man must breathe compressed air in the course of building bridges or tunnels, or when he dives deep into the sea to harvest its resources.

The term osteonecrosis is, in the opinion of the Chairmen of thes Symposium, currently the most widely accepted and the least ambiguous term available to describe the disease. It has also been known by a wide wariety of other names -- e.g., aseptic, avascular, and ischemic necrisis of bone. The term dysbaric osteonecrosis identifies the particular disease process found in otherwise healthy laborers who work in compressed air. It is found as well in aviators and in divers who breathe air, oxygen-helium or other gases under water. Dysbaric distinguishes the condition from the radiologically and histologically similar one found in persons known to be suffering from various chronic illnesses and from the relatively rare so-called ideopathic form of osteonecrosis. Further, the term is chosen carefully so that both bypobaric and hyperbaric workers may be included. This usage precludes scientific prejudgement regarding whether the etiological factors are associated with compression, exposure, decompression, or any other features unique to these occupations.

This Symposium sets out to define for the National Institute for Occupational Safety and Health the epidemiology of the type of osteonecrosis that develops under conditions of hyperbaric exposure. The disease is commonly described in terms of abmormalities revealed radiologically, either an increase or decrease in bone density. But a roetgenogram does not describe the disease process in pathologic terminology. A further purpose of this Symposium, then, is to detail the relationship between dysbarism and osteonecrosis, the disease process, and its etiology (at least the theories conrcerning the cause of osteonecrosis).

The prevention of osteonecrosis is, quite naturally, the most important subject of the Symposium. One can hardly recommend that there be no more diving, although those who are never exposed to hyperbaric or reduced pressure do not develop dysbarism-related osteonecrosis. Since no consensus exists on the subjects of etiology, prevention, exacerbating conditions, or management of the disease, once it occurs, it becomes obvious that additional research must be conducted to answer these crucial questions.

It is the belief of the Chairmen that this, the proceedings of the first symposium on the subject, will prove to be of value for several years to come for both the participants and those who were unable to attend.

Edward L. Beckman
David H. Elliott
Symposium Chairmen

I will only quote about three more paragraphs, then discuss what has been written:

OSTEONECROSIS IN TUNNEL AND CAISSON WORKERS
R. Ian McCallum

...The first British radiographic survey of the joints of men during the course of their employment in compressed air, at the Dartford Tunnel, was a rather limited one (Golding et al., 1960). At this contract the primary interest of the DSP was to evaluate what was at that time a new decompression table (Work in Compressed Air Special Regulations, 1958), a table that is in fact still the official one in Great Britain. Symptomless bone necrosis was found in 10 out of 83 men with a long history of exposure to cempressed air, all of whom had suffered from bends at one time or another; and in 3 of 20 men who had never sought treatment for decompression sickness. It was thus estabilshed that a history of bends severe enough to demand treatment is not necessarily associated with bone necrosis.

It became clear that for practical pruposes radiography of the bones of compressed-air workers should be concentrated on the areas around the shoulder, hip, and knee joints. THese sites, particularly the hips and shoulders, are the clinically important ones. Radiation exposure in routine examinations had to be limited; and the time involved in these examinations, which were and are still voluntary in the U.K., further restricted the number of radiographs taken.

...These considerations were applied in a study of men employed in compressed air during the construction of two tunnels under the river Clyde in Glasgow (Decompression Sickness Panel, 1966). Work on these tunnels was spread over five years, during which time 1362 men were so employed. In this suvey 47 (19%) of the 241 men radiographed were found to have one or more bone lesions. subsequently 11 other men not included inthe original survey were found to have bone lesions. Out of 58 men known to have developed bone necrosis during this contract, 12 have become seriously disabled by lesions in the femoral or humeral heads...

DECOMPRESSION TABLES IN RELATION TO BYSBARIC OSTEONECROSIS
Claude A. Harvey

SUMMARY

In areas of developing dysbaric osteonecrosis, bone marrow probably exchanges inert gas slowly. Lesions have developed even with tables of apparent safety -- as evaluated in terms of incidence of dysbarism or by a simple expoential gas-exchange model (as used in the modified Haldane prefusion-limited model). Inequality in gas uptake and elimination, as well as the low tolerance of bone for inert-gas supersaturation, may precipitate development of lesions when present-day decompression tables are followed. Showers of silent embolic bubbles during repeated decompressions may also be contributory factors, possibly because of secondary changes in blood constituents. Reflex circulatory and toxic changes in bone from an elevated PO2 need further evaluation. Inert-gas exchange rates and the conesquences of mixing or switching inert gases should also be studied in many tissues.

A resonable approach to the modification of current decompression practices might reasonably include 1) more positive consideration of tissues with longer hald-times; 2) reduction of supersaturation in those tissues; and 3) preater emphasis on the ineqality of inert-gas uptake and elimination. Of possibel importance, as well, would be efforts to decrease the separation of gas from solution into a gas phase (siletn bubbles) by using deeper decompression stages, by closer adherence to the O2 window principle of decompression, and by monitoring with ultrasonic techniques -- particularly in repetitive diving.

However, expenditures of large amounts of time, money, and energy required to arbitrarily modify and retest existing tables seems inefficient until a better understanding of pathophysiology of dysbaric osteonecrosis helps reduce the choice of modifications. Meanwhile, a central registry to collect data on cases in the United States would allow a better evaluation of existing decompression tables. Statistical relationships could be established that might suggest certain changes that would make exsiting tables safer.

ADDITIONAL DIAGNOSTIC TECHNIQUES
John Paul Jones, Jr.

SUMMARY

When a comprehensive clinical history and physical examination indicate possible ideopathic or nontramatic osseous avascular necrosis, addidional diagnostic tests are often recommended, including tomography and radionuclide bone scans. The suspected lesion may be confirmed by various tests, such as a differential radioactive phosphorus (32P) uptake study, differential oximetry, intramedullary pressure determinations, intraosseous phlebography, and biopsy for tissue microscopy and microroentgenography.

SeaRat

 

[John C. Ratliff]

Well, my post became too long. Here's the rest of it:

Okay, I got three quotes in before my wife got home. Anyway, some of these concerns are why I have, for quite some time now, been questioning the DIR divers who dive deep, use repetitive decompression, and seem to be pushing the limits. They are risking their health in the long term.

I'll let you read this, then any more discussion can occur beyond this. But OldMossBack, the diagnisis used to be with radiography (X-rays). That was in 1974. This reference, while the first symposium, is undoubtedly badly outdated. But it did explain some of what the concerns are with this diving disease. We have developed much better diagnostic techniques since that time, and it would behoove you to seek out a diving doctor (probably through DAN) to work with and diagnose whether you have this condition or not.

SeaRat

 

[John C. Ratliff]

If you do a Google search on "Dysbarism-related Osteonecrosis" you can find a number of citations, including references to the one I posted above. One PDF to download is titled "The Depth and Gas Delemma" by Lee H. Sommers, PhD. This has a very good discussion of the topic:

PDF] THE DEPTH AND GAS DILEMMA
File Format: PDF/Adobe Acrobat - View as HTML
... Beckman, E. and Elliot, D., Dysbarism-Related Osteonecrosis (Washington:
National Institute for. Occupational Safety and Health, 1974). ...
www.oseh.umich.edu/gasdilemma.pdf - Similar*pages

The other one I saw was from the journal, Skeletal Radiology:

Publisher:*Springer-Verlag GmbH
ISSN:*0364-2348 (Paper) 1432-2161 (Online)
DOI:*10.1007/s002560050247
Issue:*Volume 26, Number 6
Date:* June 1997
Pages:*354 - 359
Magnetic resonance imaging of osteonecrosis in divers: comparison with plain radiographs


S. Shinoda , Y. Hasegawa A3, S. Kawasaki A1, N. Tagawa A1, H. Iwata A3

A1*Department of Orthopaedic Surgery, Atsumi Hospital, 27 Tsukidashi, Tahara, Tahara-cho, Atsumi-gun, Aichi-ken, 441-34 Japan
A2*Department of Orthopaedic Surgery, Aichi-ken Saiseikai Hospital, 1-1-18 Sako, Nishi-ku, Nagoya 451, Japan
A3*Department of Orthopaedic Surgery, Nagoya University School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya 466, Japan

Abstract:

Abstract Objective. To assess the diagnostic value of magnetic resonance imaging (MRI) as compared with radiographic findings in osteonecrosis in divers. Design and patients. MRI scans and conventional radiographs of the shoulder, hip and knee joints of 23 professional male scuba divers were reviewed together with their clinical findings and personal histories. Correlations between the MRI findings and the radiographic evaluation, clinical symptoms, and personal history were then investigated. Results and conclusions. Lesions found on MRI in 23 divers included 27 in 39 proximal humeri, 17 in 36 proximal femora, 13 in 32 distal femora, and 12 in 32 proximal tibiae. Diffuse, marginated, or irregular patterns were observed. No lesions were seen in epiphyses of the distal femur or proximal tibia. We tried to classify these MRI findings by location and appearance. MRI showed no patients with only one affected bone. A close correlation between the MRI findings and maximum diving depth was observed in the proximal humerus. MRI depicted bone lesions that could not be detected on the radiographs. A routine MRI investigation of the hip joints should be performed in every diver in whom osteonecrosis is diagnosed at another site, for early detection of femoral head osteonecrosis. MRI of the shoulder joint is also the best surveillance in divers who dive deeper than 15rm.

Keywords:

Key words MRI · Dysbaric osteonecrosis

The references of this article are secured to subscribers.

I talked to my wife, who is a PharmD (Doctor of Pharamcy), who said that it really doesn't matter how you get osteonecrosis, any osteopath (bone doc) should be able to diagnose and treat it.

Good luck,

SeaRat

 

[lamont]

What do you think of the theory that silent bubbles of N2 affect red blood cells to give a temporary DIY sickle cell condition -- the red blood cells then block capillaries and cause the necrosis? Also, given the belief that fatigue is a symptom of silent bubbles, that would suggest that post-dive fatigue is an indication of possible damage?

 

[John C. Ratliff]

I would say simply that I don't know. I'd look at the research and read what it said. There is a lot of "stuff" out there that may or may not be true. If it is in a peer-reviewed medical journal, a NIOSH publication, or something with some authority, then I'd be more inclined to believe it.

SeaRat